2,442 results match your criteria Apoptosis[Journal]


The specific PKC-α inhibitor chelerythrine blunts costunolide-induced eryptosis.

Apoptosis 2020 Jul 7. Epub 2020 Jul 7.

Department of Dermatology and Allergology, School of Medicine, Technical University of Munich, Biedersteinerstr. 29, 80802, München, Germany.

Costunolide, a natural sesquiterpene lactone, has multiple pharmacological activities such as neuroprotection or induction of apoptosis and eryptosis. However, the effects of costunolide on pro-survival factors and enzymes in human erythrocytes, e.g. Read More

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http://dx.doi.org/10.1007/s10495-020-01620-6DOI Listing

Elevated IL-22 in psoriasis plays an anti-apoptotic role in keratinocytes through mediating Bcl-xL/Bax.

Apoptosis 2020 Jul 6. Epub 2020 Jul 6.

Department of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

IL-22 is known to mediate inflammation in psoriasis, while IL-22 binding protein (IL-22BP) binds IL-22 to suppress IL-22 signaling. However, the function of IL-22 in regulating apoptosis in psoriasis remains poorly understood. In this study, we found that IL-22/IL-22R1 in lesional skin and IL-22 in serum from psoriatic patients were highly upregulated compared with healthy controls, while IL-22BP was not changed. Read More

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http://dx.doi.org/10.1007/s10495-020-01623-3DOI Listing

Cytokine regulation of apoptosis-induced apoptosis and apoptosis-induced cell proliferation in vascular smooth muscle cells.

Apoptosis 2020 Jul 5. Epub 2020 Jul 5.

Division of Cardiovascular Medicine, University of Cambridge, ACCI, Addenbrooke's Hospital, Box 110, CB2 0QQ, Cambridge, UK.

Vascular smooth muscle cells (VSMCs) are the main structural cell of blood vessels, and VSMC apoptosis occurs in vascular disease, after injury, and in vessel remodeling during development. Although VSMC apoptosis is viewed as silent, recent studies show that apoptotic cells can promote apoptosis-induced compensatory proliferation (AICP), apoptosis-induced apoptosis (AIA), and migration of both local somatic and infiltrating inflammatory cells. However, the effects of VSMC apoptosis on adjacent VSMCs, and their underlying signaling and mechanisms are unknown. Read More

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http://dx.doi.org/10.1007/s10495-020-01622-4DOI Listing

Rational design of genetically encoded reporter genes for optical imaging of apoptosis.

Apoptosis 2020 Aug;25(7-8):459-473

Institute of Medical Research, Northwestern Polytechnical University, Xi'an, 710072, China.

Apoptosis is a process in which cells are genetically regulated to cause a series of changes in morphology and metabolic activity, which ultimately lead to cell death. Apoptosis plays a vital role in the entire life cycle of an organism. Too much or too little apoptosis can cause a variety of diseases. Read More

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http://dx.doi.org/10.1007/s10495-020-01621-5DOI Listing

Antiproliferative effect of bacterial cyclodipeptides in the HeLa line of human cervical cancer reveals multiple protein kinase targeting, including mTORC1/C2 complex inhibition in a TSC1/2-dependent manner.

Apoptosis 2020 Jul 2. Epub 2020 Jul 2.

Laboratorio de Biotecnología Microbiana, Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, 58030, Morelia, Michoacán, México.

Cervix adenocarcinoma rendered by human papillomavirus (HPV) integration is an aggressive cancer that occurs by dysregulation of multiple pathways, including oncogenes, proto-oncogenes, and tumor suppressors. The PI3K/Akt/mTOR pathway, which cross-talks with the Ras-ERK pathway, has been associated with cervical cancers (CC), which includes signaling pathways related to carcinoma aggressiveness, metastasis, recurrence, and drug resistance. Since bacterial cyclodipeptides (CDPs) possess cytotoxic properties in HeLa cells with inhibiting Akt/S6k phosphorylation, the mechanism of CDPs cytotoxicity involved was deepened. Read More

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http://dx.doi.org/10.1007/s10495-020-01619-zDOI Listing

Cardiac Mitochondrial PTEN-L determines cell fate between apoptosis and survival during chronic alcohol consumption.

Apoptosis 2020 Aug;25(7-8):590-604

Cardiac Hypertrophy Laboratory, Department of Molecular Biology, School of Biological Sciences, Madurai Kamaraj University, Madurai, 625 021, Tamil Nadu, India.

Chronic alcohol consumption induces myocardial damage and a type of non-ischemic cardiomyopathy termed alcoholic cardiomyopathy, where mitochondrial ultrastructural damages and suppressed fusion activity promote cardiomyocyte apoptosis. The aim of the present study is to determine the role of mitochondrial fission proteins and/or other proteins that localise on cardiac mitochondria for apoptosis upon ethanol consumption. In vivo and in vitro chronic alcohol exposure increased mitochondrial Drp1 levels but knockdown of the same did not confer cardioprotection in H9c2 cells. Read More

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http://dx.doi.org/10.1007/s10495-020-01616-2DOI Listing

The therapeutic strategy of drug re-positioning to induce autophagic cell death in brain malignancy.

Authors:
Go J Yoshida

Apoptosis 2020 Aug 24;25(7-8):457-458. Epub 2020 Jun 24.

Department of Immunological Diagnosis, Juntendo University School of Medicine, Bunkyo-ku, Japan.

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http://dx.doi.org/10.1007/s10495-020-01617-1DOI Listing

The α7 and β2 nicotinic acetylcholine receptor subunits regulate apoptosis in the infant hippocampus, and in sudden infant death syndrome (SIDS).

Apoptosis 2020 Aug;25(7-8):574-589

Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, Medical Foundation Building K25, Sydney, NSW, 2006, Australia.

Apoptosis is increased in the hippocampus of infants who died of sudden infant death syndrome (SIDS), yet it is not known via which mechanism this has occurred. Following existing support for a role of the α7 and β2 nicotinic acetylcholine receptor (nAChR) subunits in apoptotic regulation, we aimed to determine whether these subunits are altered in the SIDS hippocampus and if they are correlated with cell death markers of active caspase-3 (Casp-3) and TUNEL. Further analyses were run according to the presence of major SIDS risk factors related to hypoxia (bed-sharing and prone sleeping), infection (presence of an upper respiratory tract infection (URTI)), cigarette smoke exposure and gender. Read More

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http://dx.doi.org/10.1007/s10495-020-01618-0DOI Listing

The pro-apoptotic ARTS protein induces neutrophil apoptosis, efferocytosis, and macrophage reprogramming to promote resolution of inflammation.

Apoptosis 2020 Aug;25(7-8):558-573

The Laboratory for molecular Pathways in the Resolution of Inflammation, Department of Human Biology and Medical Sciences, University of Haifa, 31905, Haifa, Israel.

ARTS (Sept4_i2) is a pro-apoptotic protein and a product of the Sept4 gene. ARTS acts upstream of mitochondria to initiate caspase activation. ARTS induces apoptosis by specifically binding XIAP and allowing de-repression of active caspases required for Mitochondrial Outer Membrane Permeabilzation (MOMP). Read More

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http://dx.doi.org/10.1007/s10495-020-01615-3DOI Listing

Cytosolic DNA sensing through cGAS and STING is inactivated by gene mutations in pangolins.

Apoptosis 2020 Aug;25(7-8):474-480

Department of Dermatology, Medical University of Vienna, Vienna, Austria.

The release of DNA into the cytoplasm upon damage to the nucleus or during viral infection triggers an interferon-mediated defense response, inflammation and cell death. In human cells cytoplasmic DNA is sensed by cyclic GMP-AMP Synthase (cGAS) and Absent In Melanoma 2 (AIM2). Here, we report the identification of a "natural knockout" model of cGAS. Read More

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http://dx.doi.org/10.1007/s10495-020-01614-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7291609PMC

Flow cytometric detection of hyper-polarized mitochondria in regulated and accidental cell death processes.

Authors:
G Warnes

Apoptosis 2020 Aug;25(7-8):548-557

Flow Cytometry Core Facility, The Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary London University, 4 Newark Street, London, E1 2AT, UK.

Shikonin induced necroptosis in Jurkat cells were identified flow cytometrically by the up-regulation of RIP3 in live cells and that a proportion of these cells underwent other forms of regulated cell death (RCD) which included parthanatos (< 10%), or cleaved PARP (< 10%) and DNA Damage (> 30%). Live necroptotic cells also possessed functioning mitochondria with hyper-polarized mitochondria membrane potential and generated a fivefold increase in cellular reactive oxygen species (ROS) which was resistant to inhibition by zVAD and necrostatin-1 (Nec-1). After loss of plasma membrane integrity these dead necroptotic cells then showed a higher incidence of parthanatos (> 40%), or cleaved PARP (> 15%) but less DNA Damage (< 15%). Read More

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http://dx.doi.org/10.1007/s10495-020-01613-5DOI Listing

Combination of a p53-activating CP-31398 and an MDM2 or a FAK inhibitor produces growth suppressive effects in mesothelioma with wild-type p53 genotype.

Apoptosis 2020 Aug;25(7-8):535-547

Division of Pathology and Cell Therapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, Chiba, 260-8717, Japan.

A majority of mesothelioma had the wild-type p53 genotype but was defective of p53 functions primarily due to a genetic defect in INK4A/ARF region. We examined a growth suppressive activity of CP-31398 which was developed to restore the p53 functions irrespective of the genotype in mesothelioma with wild-type or mutated p53. CP-31398 up-regulated p53 levels in cells with wild-type p53 genotype but induced cell growth suppression in a p53-independent manner. Read More

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http://dx.doi.org/10.1007/s10495-020-01612-6DOI Listing

Activation of β1 integrins and caveolin-1 by TF/FVIIa promotes IGF-1R signaling and cell survival.

Apoptosis 2020 Aug;25(7-8):519-534

Department of Medical Sciences, Clinical Chemistry and Science for Life Laboratory, Uppsala University Hospital, Entr. 61 3rd floor, 751 85, Uppsala, Sweden.

The tissue factor/coagulation factor VIIa (TF/FVIIa) complex induces transactivation of the IGF-1 receptor (IGF-1R) in a number of different cell types. The mechanism is largely unknown. The transactivation leads to protection from apoptosis and nuclear translocation of the IGF-1R. Read More

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http://dx.doi.org/10.1007/s10495-020-01611-7DOI Listing

Smac mimetics can provoke lytic cell death that is neither apoptotic nor necroptotic.

Apoptosis 2020 Aug;25(7-8):500-518

Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, 3086, Australia.

Smac mimetics, or IAP antagonists, are a class of drugs currently being evaluated as anti-cancer therapeutics. These agents antagonize IAP proteins, including cIAP1/2 and XIAP, to induce cell death via apoptotic or, upon caspase-8 deficiency, necroptotic cell death pathways. Many cancer cells are unresponsive to Smac mimetic treatment as a single agent but can be sensitized to killing in the presence of the cytokine TNFα, provided either exogenously or via autocrine production. Read More

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http://dx.doi.org/10.1007/s10495-020-01610-8DOI Listing

Upregulation of microRNA-532 enhances cardiomyocyte apoptosis in the diabetic heart.

Apoptosis 2020 Jun;25(5-6):388-399

Department of Physiology-HeartOtago, School of Biomedical Sciences, University of Otago, 270, Great King Street, Dunedin, 9016, New Zealand.

Type 2 diabetes has a strong association with the development of cardiovascular disease, which is grouped as diabetic heart disease (DHD). DHD is associated with the progressive loss of cardiovascular cells through the alteration of molecular signalling pathways associated with cell death. In this study, we sought to determine whether diabetes induces dysregulation of miR-532 and if this is associated with accentuated apoptosis. Read More

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http://dx.doi.org/10.1007/s10495-020-01609-1DOI Listing

Doxorubicin sensitizes cancer cells to Smac mimetic via synergistic activation of the CYLD/RIPK1/FADD/caspase-8-dependent apoptosis.

Apoptosis 2020 Jun;25(5-6):441-455

Center of Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medial College, Beijing, China.

Smac/Diablo is a pro-apoptotic protein via interaction with inhibitors of apoptosis proteins (IAPs) to relieve their inhibition of caspases. Smac mimetic compounds (also known as antagonists of IAPs) mimic the function of Smac/Diablo and sensitize cancer cells to TNF-induced apoptosis. However, the majority of cancer cells are resistant to Smac mimetic alone. Read More

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http://dx.doi.org/10.1007/s10495-020-01604-6DOI Listing

A potent protective effect of baicalein on liver injury by regulating mitochondria-related apoptosis.

Apoptosis 2020 Jun;25(5-6):412-425

Institute for Translational Medicine, Qingdao University, #38 Dengzhou Road, Qingdao, 266000, Shandong, People's Republic of China.

Liver injury is the early stage of liver disease, which is caused by multiple factors. Baicalein has shown extensive bioactivity. But whether baicalein has a protective effect on liver injury has not been reported thus far. Read More

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http://dx.doi.org/10.1007/s10495-020-01608-2DOI Listing
June 2020
3.685 Impact Factor

Hemocompatible LAT1-inhibitor can induce apoptosis in cancer cells without affecting brain amino acid homeostasis.

Apoptosis 2020 Jun;25(5-6):426-440

School of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, P.O. Box 1627, Kuopio, 70211, Finland.

Increased amounts of amino acids are essential for cancer cells to support their sustained growth and survival. Therefore, inhibitors of amino acid transporters, such as L-type amino acid transporter 1 (LAT1) have been developed. In this study, a previously reported LAT1-inhibitor (KMH-233) was studied for its hemocompatibility and toxicity towards human umbilical vein endothelial cells (HUVEC) and human aortic smooth muscle cells (AoSMCs). Read More

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http://dx.doi.org/10.1007/s10495-020-01603-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244471PMC

Gedunin isolated from the mangrove plant Xylocarpus granatum exerts its anti-proliferative activity in ovarian cancer cells through G2/M-phase arrest and oxidative stress-mediated intrinsic apoptosis.

Apoptosis 2020 Aug;25(7-8):481-499

Electron Microscopy Unit, Sophisticated Analytical Instrument Facility and Research, CSIR - Central Drug Research Institute, Sector-10, Jankipuram Extension, Lucknow, Uttar Pradesh, 226 031, India.

Gedunin is a natural tetranorterpenoid secondary metabolite found in plants of the Meliaceae family, which has been reported for its antiparasitic, antifungal and anticancer activities. Here, we describe the molecular mechanisms underlying the in vitro anti proliferative activity of gedunin (isolated from the mangrove plant Xylocarpus granatum) in human ovarian cancer cells. We observed that gedunin triggered severe ROS generation leading to DNA damage and cell cycle arrest in G2/M phase thus inhibiting cell proliferation. Read More

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http://dx.doi.org/10.1007/s10495-020-01605-5DOI Listing
August 2020
3.685 Impact Factor

Citarinostat and Momelotinib co-target HDAC6 and JAK2/STAT3 in lymphoid malignant cell lines: a potential new therapeutic combination.

Apoptosis 2020 Jun;25(5-6):370-387

Unit of Oncohematology and Osteoncology, Department of Medical and Surgical Sciences, University of Modena and Reggio Emilia, Modena, Italy.

Histone deacetylase (HDAC) inhibitors represent an encouraging class of antitumor drugs. HDAC inhibitors induce a series of molecular and biological responses and minimal toxicity to normal cells. Citarinostat (Acy-241) is a second generation, orally administered, HDAC6-selective inhibitor. Read More

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http://dx.doi.org/10.1007/s10495-020-01607-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244621PMC

The function of RNase L and its degradation mechanism in cardiac acute ischemic injury.

Apoptosis 2020 Jun;25(5-6):400-411

Department of Cardiology, Chinese PLA General Hospital, No. 28 Fuxing Road, Beijing, 100853, China.

RNase L is generally thought to play a key role in antiviral defenses. Although RNase L protein and mRNA are known to be highly expressed in myocardial tissue, there are few studies of the potential functions of RNase L in myocardial tissue. In this study, we tested the hypothesis that RNase L may be involved in the pathological process of cardiac ischemic injury. Read More

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http://dx.doi.org/10.1007/s10495-020-01606-4DOI Listing
June 2020
3.685 Impact Factor

Baicalein attenuates caspase-independent cells death via inhibiting PARP-1 activation and AIF nuclear translocation in cerebral ischemia/reperfusion rats.

Apoptosis 2020 Jun;25(5-6):354-369

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.

It is reported that baicalein can activate PI3K/AKT pathway, inhibit caspase activation and reduce cerebral infarct volume in middle cerebral artery occlusion (MCAO) rats. However, a caspase-independent mechanism initiated by poly (ADP-ribose) polymerase-1 (PARP-1) activation has been reported to make more contribution to cells death after ischemic stroke. In the present study, we established a cerebral ischemia/reperfusion (I/R) rat model through middle cerebral artery occlusion following reperfusion to investigate the mechanisms of ischemic tissue recovery following baicalein treatment. Read More

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http://dx.doi.org/10.1007/s10495-020-01600-wDOI Listing

BCL-2 family deregulation in colorectal cancer: potential for BH3 mimetics in therapy.

Apoptosis 2020 Jun;25(5-6):305-320

Laboratory for Experimental Oncology and Radiobiology, Center for Experimental and Molecular Medicine, Cancer Center Amsterdam, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.

Apoptosis is a form of programmed cell death that is essential for tissue homeostasis. De-regulation of the balance between proliferation and apoptosis contributes to tumor initiation. Particularly in the colon where apoptosis is a crucial process in intestinal turnover, inhibition of apoptosis facilitates transformation and tumor progression. Read More

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http://dx.doi.org/10.1007/s10495-020-01601-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244464PMC

Soluble receptor for advanced glycation end-products promotes angiogenesis through activation of STAT3 in myocardial ischemia/reperfusion injury.

Apoptosis 2020 Jun;25(5-6):341-353

Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, No. 119 South 4th Ring West Road, Fengtai District, Beijing, 100070, People's Republic of China.

Soluble receptor for advanced glycation end-products (sRAGE), which exerts cardioprotective effect through inhibiting cardiomyocyte apoptosis and autophagy during ischemia/reperfusion (I/R) injury, is also known to enhance angiogenesis in post-ischemic reperfusion injury-critical limb ischemia (PIRI-CLI) mice. However, whether sRAGE protects the heart from myocardial I/R injury via promoting angiogenesis remains unclear. Myocardial model of I/R injury was conducted by left anterior descending (LAD) ligation for 30 min and reperfusion for 2 weeks in C57BL/6 mice. Read More

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http://dx.doi.org/10.1007/s10495-020-01602-8DOI Listing
June 2020
3.685 Impact Factor

miR-21 protects neonatal rats from hypoxic-ischemic brain damage by targeting CCL3.

Apoptosis 2020 04;25(3-4):275-289

Outpatient Department of Pediatrics, The First Hospital of Jilin University, No. 1, Xinmin Street, Changchun, 130021, Jilin Province, People's Republic of China.

Hypoxic-ischemic brain damage (HIBD) represents one of the leading causes of neonatal mortality and permanent neurological disability worldwide. Compelling studies have identified implication of microRNAs (miRNAs) in HIBD. However, the molecular mechanism of miR-21 underlying the disease pathogenesis is unknown. Read More

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http://dx.doi.org/10.1007/s10495-020-01596-3DOI Listing

Glucocorticoid-induced autophagy and apoptosis in bone.

Apoptosis 2020 04;25(3-4):157-168

Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People's Republic of China.

Glucocorticoids are widely prescribed to treat various allergic and autoimmune diseases; however, long-term use results in glucocorticoid-induced osteoporosis, characterized by consistent changes in bone remodeling with decreased bone formation as well as increased bone resorption. Not only bone mass but also bone quality decrease, resulting in an increased incidence of fractures. The primary role of autophagy is to clear up damaged cellular components such as long-lived proteins and organelles, thus participating in the conservation of different cells. Read More

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http://dx.doi.org/10.1007/s10495-020-01599-0DOI Listing

Programmed death, cells on the last train to glory.

Apoptosis 2020 04;25(3-4):151-153

Angiogenesis Laboratory, Department of Medical Oncology, Amsterdam UMC, Cancer Center Amsterdam, 1081 HV, Amsterdam, The Netherlands.

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http://dx.doi.org/10.1007/s10495-020-01598-1DOI Listing

Abdominal paracentesis drainage attenuates severe acute pancreatitis by enhancing cell apoptosis via PI3K/AKT signaling pathway.

Apoptosis 2020 04;25(3-4):290-303

Department of General Surgery &, Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command (Chengdu Military General Hospital), Chengdu, 610083, China.

Our previous studies have shown that abdominal paracentesis drainage (APD) is a safe and effective strategy for patients with severe acute pancreatitis (SAP). However, the underlying mechanisms behind APD treatment remain poorly understood. Given that apoptosis is a critical pathological response of SAP, we here aim to investigate the effect of APD on cell apoptosis in pancreatic tissues during SAP and to explore its potential molecular mechanism. Read More

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http://dx.doi.org/10.1007/s10495-020-01597-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7181427PMC

BRAFi induced demethylation of miR-152-5p regulates phenotype switching by targeting TXNIP in cutaneous melanoma.

Apoptosis 2020 04;25(3-4):179-191

Department of Plastic Surgery, the First Affiliated Hospital of China Medical University, No.155, Nanjing North Street, Shenyang City, 110001, Liaoning, China.

Treatment of advanced BRAF-mutant melanoma using BRAF inhibitors (BRAFi) eventually leads to drug resistance and selects for highly metastatic tumor cells. We compared the most differentially dysregulated miRNA expression profiles of vemurafenib-resistant and highly-metastatic melanoma cell lines obtained from GEO DataSets. We discovered miR-152-5p was a potential regulator mediating melanoma drug resistance and metastasis. Read More

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http://dx.doi.org/10.1007/s10495-019-01586-0DOI Listing

Exploitation of a novel phenothiazine derivative for its anti-cancer activities in malignant glioblastoma.

Apoptosis 2020 04;25(3-4):261-274

Division of Cell Biology, Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, Cape Town, 7925, South Africa.

Glioblastoma remains the most malignant of all primary adult brain tumours with poor patient survival and limited treatment options. This study adopts a drug repurposing approach by investigating the anti-cancer activity of a derivative of the antipsychotic drug phenothiazine (DS00329) in malignant U251 and U87 glioblastoma cells. Results from MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and clonogenic assays showed that DS00329 inhibited short-term glioblastoma cell viability and long-term survival while sparing non-cancerous cells. Read More

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http://dx.doi.org/10.1007/s10495-020-01594-5DOI Listing

Potent antitumor activity of oncolytic adenovirus expressing C/EBPβ against hepatocellular carcinoma.

Apoptosis 2020 04;25(3-4):154-156

Hebi Precision Medical Research Institute, People's Hospital of Hebi, 412 Hemei Boulevard, Hebi, 458030, Henan Province, China.

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http://dx.doi.org/10.1007/s10495-020-01595-4DOI Listing

Synergism of 4HPR and SAHA increases anti-tumor actions in glioblastoma cells.

Apoptosis 2020 04;25(3-4):217-232

Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Columbia, SC, 29209, USA.

Glioblastoma is the most malignant and prevalent brain tumor in adults. It can grow and spread quickly causing harm to the brain health. One of the major challenges in treatment of glioblastoma is drug resistance. Read More

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http://dx.doi.org/10.1007/s10495-020-01590-9DOI Listing

Loss of BIM in T cells results in BCL-2 family BH3-member compensation but incomplete cell death sensitivity normalization.

Apoptosis 2020 04;25(3-4):247-260

Department of Pediatrics, Section of Hematology/Oncology, University of Chicago, 900 East 57th Street, KCBD 5122, Chicago, IL, 60637, USA.

BIM is the master BH3-only BCL-2 family regulator of lymphocyte survival. To understand how long-term loss of BIM affects apoptotic resistance in T cells we studied animals with T cell-specific deletion of Bim. Unlike CD19Bim animals, LCKBim mice have pronounced early lymphocytosis followed by normalization of lymphocyte counts over time. Read More

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http://dx.doi.org/10.1007/s10495-020-01593-6DOI Listing

Lactate accelerates vascular calcification through NR4A1-regulated mitochondrial fission and BNIP3-related mitophagy.

Apoptosis 2020 Jun;25(5-6):321-340

Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, 210009, People's Republic of China.

Arterial media calcification is related to mitochondrial dysfunction. Protective mitophagy delays the progression of vascular calcification. We previously reported that lactate accelerates osteoblastic phenotype transition of VSMC through BNIP3-mediated mitophagy suppression. Read More

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http://dx.doi.org/10.1007/s10495-020-01592-7DOI Listing

DDX3 modulates cisplatin resistance in OSCC through ALKBH5-mediated mA-demethylation of FOXM1 and NANOG.

Apoptosis 2020 04;25(3-4):233-246

Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar, Odisha, 751023, India.

Platinum based drugs alone or in combination with 5FU and docetaxel are common regimen chemotherapeutics for the treatment of advanced OSCC. Chemoresistance is one of the major factors of treatment failure in OSCC. Human RNA helicase DDX3 plays an important role in cell proliferation, invasion, and metastasis in several neoplasms. Read More

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http://dx.doi.org/10.1007/s10495-020-01591-8DOI Listing

microRNA-499a promotes the progression and chemoresistance of cervical cancer cells by targeting SOX6.

Apoptosis 2020 04;25(3-4):205-216

MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou, 510631, Guangdong, China.

Emerging evidence has indicated that microRNAs are involved in multiple processes of cancer development. Previous studies have demonstrated that microRNA-499a (miR-499a) plays both oncogenic and tumor suppressive roles in several types of malignancies, and genetic variants in miR-499a are associated with the risk of cervical cancer. However, the biological roles of miR-499a in cervical cancer have not been investigated. Read More

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http://dx.doi.org/10.1007/s10495-019-01588-yDOI Listing

Necroptosis and its role in infectious diseases.

Apoptosis 2020 04;25(3-4):169-178

Post-Doctoral Research Station, Henan Agriculture University, No. 63, Nonye Road, Zhengzhou, 450002, People's Republic of China.

Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). Read More

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http://dx.doi.org/10.1007/s10495-019-01589-xDOI Listing

PDGFRβ-targeted TRAIL specifically induces apoptosis of activated hepatic stellate cells and ameliorates liver fibrosis.

Apoptosis 2020 02;25(1-2):105-119

Key Lab of Transplant Engineering and Immunology, MOH; Regenerative Medical Research Center, West China Hospital, Sichuan University, Chengdu, 610041, China.

Liver fibrosis usually progresses to liver cirrhosis and even hepatocellular carcinoma. Since activated hepatic stellate cells (aHSCs) are responsible for liver fibrosis, reducing the quantity of aHSCs was considered the essential strategy for clinical antihepatofibrotic therapy. Due to the overexpression of TRAIL receptor 2 (DR5) in aHSCs, human TNF-related apoptosis-inducing ligand (hTRAIL) that could induce aHSCs apoptosis might be feasible for antihepatofibrotic therapy. Read More

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http://dx.doi.org/10.1007/s10495-019-01583-3DOI Listing
February 2020

Artemisinin and dihydroartemisinin promote β-cell apoptosis induced by palmitate via enhancing ER stress.

Apoptosis 2020 04;25(3-4):192-204

Department of Endocrinology, Children's Hospital of Nanjing Medical University, Guangzhou Road #72, Nanjing, 210008, China.

Artemisinin (ART) and dihydroartemisinin (DHA) are first-line antimalarial drugs and have been reported to have anti-obesity effects. Hyperlipidemia is associated with β-cell damage in obese subjects, which could contribute to the pathogenesis of type 2 diabetes. In addition to their anti-obesity effects, ART and DHA also have protective roles in some diseases. Read More

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http://dx.doi.org/10.1007/s10495-019-01587-zDOI Listing

Lysophosphatidic acid promotes survival of T lymphoma cells by altering apoptosis and glucose metabolism.

Apoptosis 2020 02;25(1-2):135-150

Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 221005, India.

Lysophosphatidic acid (LPA) is a bioactive lipid, which plays an indispensable role in various physiological and pathological processes. Moreover, an elevated level of LPA has been observed in malignancies of different origins and implicated in their progression via modulation of proliferation, apoptosis, invasion and metastasis. Interestingly, few recent reports suggest a pivotal role of LPA-modulated metabolism in oncogenesis of ovarian cancer. Read More

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http://dx.doi.org/10.1007/s10495-019-01585-1DOI Listing
February 2020
3.685 Impact Factor

Liposomal encapsulation of silver nanoparticles (AgNP) improved nanoparticle uptake and induced redox imbalance to activate caspase-dependent apoptosis.

Apoptosis 2020 02;25(1-2):120-134

School of Physics, Technological University Dublin, Kevin Street, Dublin 8, Ireland.

Macrophages play a crucial role in several diseases' development and progression, such as in cancer and arthritis through ROS generation and inflammation. This makes macrophages a therapeutic target in these diseases. While silver nanoparticles (AgNP) have been widely used as an antibacterial and investigated as anticancer, its potential against macrophages may be limited due to its inherent oxidative mechanism. Read More

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http://dx.doi.org/10.1007/s10495-019-01584-2DOI Listing
February 2020

MicroRNA-214 targets COX-2 to antagonize indoxyl sulfate (IS)-induced endothelial cell apoptosis.

Apoptosis 2020 02;25(1-2):92-104

Department of Nephrology, Children's Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, People's Republic of China.

Cardiovascular disease (CVD) serves as the major cause of mortality in chronic kidney disease (CKD) patients. The injury of endothelium associated with the long-term challenge of uremic toxins including the toxic indoxyl sulfate (IS) is one of key pathological factors leading to CVD. However, the mechanisms of uremic toxins, especially the IS, resulting in endothelial injury, remain unclear. Read More

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http://dx.doi.org/10.1007/s10495-019-01582-4DOI Listing
February 2020
3.685 Impact Factor

Correction to: M1 macrophage dependent-p53 regulates the intracellular survival of mycobacteria.

Apoptosis 2020 Feb;25(1-2):56

Department of Microbiology, College of Medicine, Chungnam National University, Daejeon, 35015, South Korea.

The original version of this article unfortunately contains an error in the acknowledgement section. The text "Brain Korea 21 PLUS Project for Medical Science, Chungnam National University" was omitted by mistake. The correct and complete acknowledgment is given below: Acknowledgments This work was supported by the research fund of Chungnam National University and the Brain Korea 21 PLUS Project for Medical Science, Chungnam National University. Read More

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http://dx.doi.org/10.1007/s10495-019-01581-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965334PMC
February 2020

Effect of miR-27b-5p on apoptosis of human vascular endothelial cells induced by simulated microgravity.

Apoptosis 2020 02;25(1-2):73-91

School of Aerospace Medicine, Fourth Military Medical University, 169 Chang Le Xi Road, Xi'an, 710032, Shaanxi, China.

Weightlessness-induced cardiovascular dysfunction can lead to physiological and pathological consequences. It has been shown that spaceflight or simulated microgravity can alter expression profiles of some microRNAs (miRNAs). Here, we attempt to identify the role of miRNAs in human umbilical vein endothelial cells (HUVECs) apoptosis under simulated microgravity. Read More

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http://dx.doi.org/10.1007/s10495-019-01580-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965346PMC
February 2020

Klotho-mediated changes in the expression of Atg13 alter formation of ULK1 complex and thus initiation of ER- and Golgi-stress response mediated autophagy.

Apoptosis 2020 02;25(1-2):57-72

Department of Animal Physiology and Reproduction, Faculty of Biotechnology, University of Rzeszow, Werynia 502, 36-100, Kolbuszowa, Poland.

In the previous paper of our group, we have demonstrated that one of the crucial factors involved in the crosstalk between autophagy and apoptosis is klotho protein. We have shown that klotho silencing in normal human fibroblasts intensifies lipopolysaccharide (LPS)-induced p-eIF2a-mediated stress of endoplasmic reticulum and thus leads to retardation of prosurvival autophagy and induction of apoptotic cell death. In this study, we have performed a detailed step-by-step analysis of autophagy flux-related genes' expression and endoplasmic reticulum and Golgi stress related pathways in order to determine the exact mechanistic event when autophagy is inhibited in klotho-deficient cells on account of apoptosis initiation. Read More

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http://dx.doi.org/10.1007/s10495-019-01579-zDOI Listing
February 2020

M1 macrophage dependent-p53 regulates the intracellular survival of mycobacteria.

Apoptosis 2020 02;25(1-2):42-55

Department of Microbiology, College of Medicine, Chungnam National University, Daejeon, 35015, South Korea.

Tumor suppressor p53 is not only affects immune responses but also contributes to antibacterial activity. However, its bactericidal function during mycobacterial infection remains unclear. In this study, we found that the p53-deficient macrophages failed to control Mycobacterium tuberculosis (Mtb), manifested as a lower apoptotic cell death rate and enhanced intracellular survival. Read More

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http://dx.doi.org/10.1007/s10495-019-01578-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965052PMC
February 2020

Influenza A virus-induced apoptosis and virus propagation.

Apoptosis 2020 02;25(1-2):1-11

Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 28 Medical Drive, Singapore, 117456, Singapore.

Influenza A viruses (IAVs) are respiratory pathogens that cause severe morbidity and mortality worldwide. They affect cellular processes such as proliferation, protein synthesis, autophagy, and apoptosis. Although apoptosis is considered an innate cellular response to invading infectious pathogens, IAVs have evolved to encode viral proteins that modulate host cellular apoptosis in ways that support efficient viral replication and propagation. Read More

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http://dx.doi.org/10.1007/s10495-019-01575-3DOI Listing
February 2020

Inhibitors of HSP90 in melanoma.

Apoptosis 2020 02;25(1-2):12-28

Department of Molecular Biology of Cancer, Medical University of Lodz, 6/8 Mazowiecka Street, 92-215, Lodz, Poland.

HSP90 (heat shock protein 90) is an ATP-dependent molecular chaperone involved in a proper folding and maturation of hundreds of proteins. HSP90 is abundantly expressed in cancer, including melanoma. HSP90 client proteins are the key oncoproteins of several signaling pathways controlling melanoma development, progression and response to therapy. Read More

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http://dx.doi.org/10.1007/s10495-019-01577-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965345PMC
February 2020

Accumulation of tissue factor in endothelial cells promotes cellular apoptosis through over-activation of Src1 and involves β1-integrin signalling.

Apoptosis 2020 02;25(1-2):29-41

Biomedical Sciences, University of Hull, Cottingham Road, Hull, HU6 7RX, UK.

Accumulation of tissue factor (TF) within cells leads to cellular apoptosis mediated through p38 and p53 pathways. In this study, the involvement of Src1 in the induction of TF-mediated cell apoptosis, and the mechanisms of Src1 activation were investigated. Human coronary artery endothelial cell (HCAEC) were transfected with plasmids to express the wild-type TF (TF-tGFP), or a mutant (Ser253 → Ala) which is incapable of being released from cells (TF-tGFP). Read More

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http://dx.doi.org/10.1007/s10495-019-01576-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965344PMC
February 2020

Integrin-EGFR interaction regulates anoikis resistance in colon cancer cells.

Apoptosis 2019 12;24(11-12):958-971

Division of Molecular Medicine, Bose Institute, P-1/12, Calcutta Improvement Trust Scheme VII M, Kolkata, 700 054, India.

Anoikis resistance is an essential property of cancer cells that allow the extra-cellular matrix-detached cells to survive in a suspended state in body fluid in order to metastasize and invade to distant organs. It is known that integrins play an important role in anoikis resistance, but detailed mechanisms are not well understood. Here we report that highly metastatic colon cancer cells showed a higher degree of anoikis resistance than the normal intestinal epithelial cells. Read More

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http://dx.doi.org/10.1007/s10495-019-01573-5DOI Listing
December 2019