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    485 results match your criteria Cell Communication and Signaling [Journal]

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    Human hyaluronic acid synthase-1 promotes malignant transformation via epithelial-to-mesenchymal transition, micronucleation and centrosome abnormalities.
    Cell Commun Signal 2017 Nov 14;15(1):48. Epub 2017 Nov 14.
    Atlantic Cancer Research Institute, 35 Providence Street, Moncton, NB, E1C 8X3, Canada.
    Background: Human hyaluronic acid (HA) molecules are synthesized by three membrane spanning Hyaluronic Acid Synthases (HAS1, HAS2 and HAS3). Of the three, HAS1 is found to be localized more into the cytoplasmic space where it synthesizes intracellular HA. HA is a ubiquitous glycosaminoglycan, mainly present in the extracellular matrix (ECM) and on the cell surface, but are also detected intracellularly. Read More

    Impaired mitochondrial calcium uptake caused by tacrolimus underlies beta-cell failure.
    Cell Commun Signal 2017 Nov 13;15(1):47. Epub 2017 Nov 13.
    Department of Medicine, Albert Einstein College of Medicine, New York, NY, USA.
    Background: One of the most common side effects of the immunosuppressive drug tacrolimus (FK506) is the increased risk of new-onset diabetes mellitus. However, the molecular mechanisms underlying this association have not been fully clarified.

    Methods: We studied the effects of the therapeutic dose of tacrolimus on mitochondrial fitness in beta-cells. Read More

    A transwell assay that excludes exosomes for assessment of tunneling nanotube-mediated intercellular communication.
    Cell Commun Signal 2017 Nov 13;15(1):46. Epub 2017 Nov 13.
    Department of Medicine, Division of Hematology, Oncology and Transplantation, University of Minnesota, Mayo Mail Code 480, 420 Delaware Street SE, Minneapolis, MN, 55455, USA.
    Background: Tunneling nanotubes (TNTs) are naturally-occurring filamentous actin-based membranous extensions that form across a wide spectrum of mammalian cell types to facilitate long-range intercellular communication. Valid assays are needed to accurately assess the downstream effects of TNT-mediated transfer of cellular signals in vitro. We recently reported a modified transwell assay system designed to test the effects of intercellular transfer of a therapeutic oncolytic virus, and viral-activated drugs, between cells via TNTs. Read More

    CD146, a novel target of CD44-signaling, suppresses breast tumor cell invasion.
    Cell Commun Signal 2017 Nov 9;15(1):45. Epub 2017 Nov 9.
    Department of Obstetrics and Gynecology, Louisiana State University, Health Sciences Center, New Orleans, USA.
    Background: We have previously validated three novel CD44-downstream positively regulated transcriptional targets, including Cortactin, Survivin and TGF-β2, and further characterized the players underlying their separate signaling pathways. In the present study, we identified CD146 as a potential novel target, negatively regulated by CD44. While the exact function of CD146 in breast cancer (BC) is not completely understood, substantial evidence from our work and others support the hypothesis that CD146 is a suppressor of breast tumor progression. Read More

    Metabolic shift in density-dependent stem cell differentiation.
    Cell Commun Signal 2017 Oct 20;15(1):44. Epub 2017 Oct 20.
    Systems Biology and Cancer Metabolism, Program for Quantitative Systems Biology, University of California Merced, 2500 North Lake Road, Merced, CA, 95343, USA.
    Background: Vascular progenitor cells (VPCs) derived from embryonic stem cells (ESCs) are a valuable source for cell- and tissue-based therapeutic strategies. During the optimization of endothelial cell (EC) inductions from mouse ESCs using our staged and chemically-defined induction methods, we found that cell seeding density but not VEGF treatment between 10 ng/mL and 40 ng/mL was a significant variable directing ESCs into FLK1(+) VPCs during stage 1 induction. Here, we examine potential contributions from cell-to-cell signaling or cellular metabolism in the production of VPCs from ESCs seeded at different cell densities. Read More

    Human umbilical cord Wharton jelly cells promote extra-pancreatic insulin formation and repair of renal damage in STZ-induced diabetic mice.
    Cell Commun Signal 2017 Oct 17;15(1):43. Epub 2017 Oct 17.
    Department of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, 515041, People's Republic of China.
    Background: We evaluated the therapeutic effect and fate of high doses of human umbilical cord Wharton jelly cells (hUCWJCs) after IP administration to streptozotocin (STZ)-induced diabetic mice.

    Methods: Type 1 diabetes (T1D) was induced in Kunming mice via IP injection of STZ. hUCWJCs were labeled with 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI). Read More

    A novel protein derived from lamprey supraneural body tissue with efficient cytocidal actions against tumor cells.
    Cell Commun Signal 2017 Oct 16;15(1):42. Epub 2017 Oct 16.
    College of Life Science, Liaoning Normal University, Dalian, 116081, China.
    Background: In previous research, we found that cell secretion from the adult lamprey supraneural body tissues possesses cytocidal activity against tumor cells, but the protein with cytocidal activity was unidentified.

    Methods: A novel lamprey immune protein (LIP) as defense molecule was first purified and identified in jawless vertebrates (cyclostomes) using hydroxyapatite column and Q Sepharose Fast Flow column. After LIP stimulation, morphological changes of tumor cells were analysed and measured whether in vivo or in vitro. Read More

    DNA damage response and cancer therapeutics through the lens of the Fanconi Anemia DNA repair pathway.
    Cell Commun Signal 2017 Oct 10;15(1):41. Epub 2017 Oct 10.
    Cold Spring Harbor Laboratory, New York, USA.
    Fanconi Anemia (FA) is a rare, inherited genomic instability disorder, caused by mutations in genes involved in the repair of interstrand DNA crosslinks (ICLs). The FA signaling network contains a unique nuclear protein complex that mediates the monoubiquitylation of the FANCD2 and FANCI heterodimer, and coordinates activities of the downstream DNA repair pathway including nucleotide excision repair, translesion synthesis, and homologous recombination. FA proteins act at different steps of ICL repair in sensing, recognition and processing of DNA lesions. Read More

    Impairment of IGF2 gene expression in prostate cancer is triggered by epigenetic dysregulation of IGF2-DMR0 and its interaction with KLF4.
    Cell Commun Signal 2017 Oct 10;15(1):40. Epub 2017 Oct 10.
    Clinic of Urology, Pediatric Urology and Andrology, Justus-Liebig-University Giessen, Rudolf-Buchheim-Str. 7, 35392, Giessen, Germany.
    Background: Human cancer cells often exhibit impaired IGF2 expression and the underlying mechanisms are multifaceted and complex. Besides the well-known imprinting control region IGF2/H19-ICR, the involvement of a differentially methylated region in the promoter P0 of IGF2 gene (IGF2-DMR0) has been suggested. Here, we evaluate several mechanisms potentially leading to up- and/or down-regulation of IGF2 expression in prostate cancer and present a novel role of Kruppel-like factor 4 (KLF4) as a transcriptional regulator of IGF2 binding in IGF2-DMR0. Read More

    NF-κB potentiates tumor growth by suppressing a novel target LPTS.
    Cell Commun Signal 2017 Oct 10;15(1):39. Epub 2017 Oct 10.
    Department of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing, 400038, China.
    Background: Chronic inflammation is causally linked to the carcinogenesis and progression of most solid tumors. LPTS is a well-identified tumor suppressor by inhibiting telomerase activity and cancer cell growth. However, whether and how LPTS is regulated by inflammation signaling is still incompletely elucidated. Read More

    CLCA1 suppresses colorectal cancer aggressiveness via inhibition of the Wnt/beta-catenin signaling pathway.
    Cell Commun Signal 2017 Oct 3;15(1):38. Epub 2017 Oct 3.
    Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, China), the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
    Background: Chloride channel accessory 1 (CLCA1) belongs to the calcium-sensitive chloride conductance protein family, which is mainly expressed in the colon, small intestine and appendix. This study was conducted to investigate the functions and mechanisms of CLCA1 in colorectal cancer (CRC).

    Methods: The CLCA1 protein expression level in CRC patients was evaluated by enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), and western blotting analysis. Read More

    Crosstalk between glial and glioblastoma cells triggers the "go-or-grow" phenotype of tumor cells.
    Cell Commun Signal 2017 Oct 2;15(1):37. Epub 2017 Oct 2.
    Life and Health Sciences Research Institute (ICVS), School of Medicine, Campus de Gualtar, University of Minho, 4710-057, Braga, Portugal.
    Background: Glioblastoma (GBM), the most malignant primary brain tumor, leads to poor and unpredictable clinical outcomes. Recent studies showed the tumor microenvironment has a critical role in regulating tumor growth by establishing a complex network of interactions with tumor cells. In this context, we investigated how GBM cells modulate resident glial cells, particularly their paracrine activity, and how this modulation can influence back on the malignant phenotype of GBM cells. Read More

    ARF1 recruits RAC1 to leading edge in neutrophil chemotaxis.
    Cell Commun Signal 2017 Oct 2;15(1):36. Epub 2017 Oct 2.
    Department of Molecular Biology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
    Background: The small GTPase ARF1 mediates membrane trafficking mostly from the Golgi, and is essential for the G protein-coupled receptor (GPCR)-mediated chemotaxis of neutrophils. In this process, ARF1 is activated by the guanine nucleotide exchanger GBF1, and is inactivated by the GTPase-activating protein GIT2. Neutrophils generate the Gβγ-PAK1-αPIX-GIT2 linear complex during GPCR-induced chemotaxis, in which αPIX activates RAC1/CDC42, which then employs PAK1. Read More

    The emerging roles of phosphatases in Hedgehog pathway.
    Cell Commun Signal 2017 Sep 20;15(1):35. Epub 2017 Sep 20.
    Institute of Evolution & Marine Biodiversity, College of Marine Life Sciences, Ocean University of China, Qingdao, 266003, China.
    Hedgehog signaling is evolutionarily conserved and plays a pivotal role in cell fate determination, embryonic development, and tissue renewal. As aberrant Hedgehog signaling is tightly associated with a broad range of human diseases, its activities must be precisely controlled. It has been known that several core components of Hedgehog pathway undergo reversible phosphorylations mediated by protein kinases and phosphatases, which acts as an effective regulatory mechanism to modulate Hedgehog signal activities. Read More

    Tissue-resident stem cell activity: a view from the adult Drosophila gastrointestinal tract.
    Cell Commun Signal 2017 Sep 18;15(1):33. Epub 2017 Sep 18.
    Department of Genetics, College of Life Sciences, Northeast Forestry University, No.26 Hexing Road Xiangfang District, Harbin, 150040, China.
    The gastrointestinal tract serves as a fast-renewing model for unraveling the multifaceted molecular mechanisms underlying remarkably rapid cell renewal, which is exclusively fueled by a small number of long-lived stem cells and their progeny. Stem cell activity is the best-characterized aspect of mucosal homeostasis in mitotically active tissues, and the dysregulation of regenerative capacity is a hallmark of epithelial immune defects. This dysregulation is frequently associated with pathologies ranging from chronic enteritis to malignancies in humans. Read More

    Osteoglycin promotes meningioma development through downregulation of NF2 and activation of mTOR signaling.
    Cell Commun Signal 2017 Sep 18;15(1):34. Epub 2017 Sep 18.
    Center for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
    Background: Meningiomas are the most common primary intracranial tumors in adults. While a majority of meningiomas are slow growing neoplasms that may cured by surgical resection, a subset demonstrates more aggressive behavior and insidiously recurs despite surgery and radiation, without effective alternative treatment options. Elucidation of critical mitogenic pathways in meningioma oncogenesis may offer new therapeutic strategies. Read More

    CRAMP deficiency leads to a pro-inflammatory phenotype and impaired phagocytosis after exposure to bacterial meningitis pathogens.
    Cell Commun Signal 2017 Sep 16;15(1):32. Epub 2017 Sep 16.
    Department of Anatomy and Cell Biology, RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
    Background: Antimicrobial peptides are important components of the host defence with a broad range of functions including direct antimicrobial activity and modulation of inflammation. Lack of cathelin-related antimicrobial peptide (CRAMP) was associated with higher mortality and bacterial burden and impaired neutrophil granulocyte infiltration in a model of pneumococcal meningitis. The present study was designed to characterize the effects of CRAMP deficiency on glial response and phagocytosis after exposure to bacterial stimuli. Read More

    Inhibition of TRPM7 suppresses cell proliferation of colon adenocarcinoma in vitro and induces hypomagnesemia in vivo without affecting azoxymethane-induced early colon cancer in mice.
    Cell Commun Signal 2017 Aug 15;15(1):30. Epub 2017 Aug 15.
    Center for Biomedical Research, The Queen's Medical Center, John A. Burns School of Medicine, University of Hawaii, 1301 Punchbowl St., Honolulu, HI, 96813, USA.
    Background: Magnesium (Mg(2+)) is an essential cation implicated in carcinogenesis, solid tumor progression and metastatic potential. The Transient Receptor Potential Melastatin Member 7 (TRPM7) is a divalent ion channel involved in cellular and systemic Mg(2+) homeostasis. Abnormal expression of TRPM7 is found in numerous cancers, including colon, implicating TRPM7 in this process. Read More

    Csk-homologous kinase (Chk) is an efficient inhibitor of Src-family kinases but a poor catalyst of phosphorylation of their C-terminal regulatory tyrosine.
    Cell Commun Signal 2017 Aug 7;15(1):29. Epub 2017 Aug 7.
    Department of Biochemistry & Molecular Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
    Background: C-terminal Src kinase (Csk) and Csk-homologous kinase (Chk) are the major endogenous inhibitors of Src-family kinases (SFKs). They employ two mechanisms to inhibit SFKs. First, they phosphorylate the C-terminal tail tyrosine which stabilizes SFKs in a closed inactive conformation by engaging the SH2 domain in cis. Read More

    Deficiency of PI3-Kinase catalytic isoforms p110γ and p110δ in mice enhances the IL-17/G-CSF axis and induces neutrophilia.
    Cell Commun Signal 2017 Jul 19;15(1):28. Epub 2017 Jul 19.
    Department of Pharmacology and Experimental Therapy, Institute of Experimental and Clinical Pharmacology and Toxicology and ICePhA mouse clinic, University of Tübingen, D-72074, Tübingen, Germany.
    Background: Phosphoinositide 3-kinase γ (PI3Kγ) and PI3Kδ are second messenger-generating enzymes with key roles in proliferation, differentiation, survival, and function of leukocytes. Deficiency of the catalytic subunits p110γ and p110δ of PI3Kγ and PI3Kδ in p110γ/δ(-/-) mice leads to defective B- and T-cell homeostasis. Here we examined the role of p110γ and p110δ in the homeostasis of neutrophils by analyzing p110γ(-/-), p110δ(-/-) and p110γ/δ(-/-) mice. Read More

    Viral manipulation of the cellular sumoylation machinery.
    Cell Commun Signal 2017 Jul 14;15(1):27. Epub 2017 Jul 14.
    Division of Biomedical Sciences, Mercer University School of Medicine, Macon, Georgia.
    Viruses exploit various cellular processes for their own benefit, including counteracting anti-viral responses and regulating viral replication and propagation. In the past 20 years, protein sumoylation has emerged as an important post-translational modification that is manipulated by viruses to modulate anti-viral responses, viral replication, and viral pathogenesis. The process of sumoylation is a multi-step cascade where a small ubiquitin-like modifier (SUMO) is covalently attached to a conserved ΨKxD/E motif within a target protein, altering the function of the modified protein. Read More

    Glyceollins trigger anti-proliferative effects through estradiol-dependent and independent pathways in breast cancer cells.
    Cell Commun Signal 2017 Jun 30;15(1):26. Epub 2017 Jun 30.
    Institut de Recherche en Santé-Environnement-Travail (IRSET), University of Rennes 1, 9 Avenue du Pr Léon Bernard, 35000, Rennes, France.
    Background: Estrogen receptors (ER) α and β are found in both women and men in many tissues, where they have different functions, including having roles in cell proliferation and differentiation of the reproductive tract. In addition to estradiol (E2), a natural hormone, numerous compounds are able to bind ERs and modulate their activities. Among these compounds, phytoestrogens such as isoflavones, which are found in plants, are promising therapeutics for several pathologies. Read More

    Fibroblast growth factor 2 supports osteoblastic niche cells during hematopoietic homeostasis recovery after bone marrow suppression.
    Cell Commun Signal 2017 Jun 29;15(1):25. Epub 2017 Jun 29.
    Department of Biochemistry, BK21 PLUS Program for Creative Veterinary Science Research and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, South Korea.
    Background: Hematopoietic stem cell (HSC) maintenance requires a specific microenvironment. HSC niches can be activated by tissue damaging chemotherapeutic drugs and various cell signaling molecules such as SDF-1 and FGF, which might also result in bone marrow stress. Recent research has insufficiently shown that endosteal osteolineage cells and other niche constituents recover after marrow injury. Read More

    Kaiso differentially regulates components of the Notch signaling pathway in intestinal cells.
    Cell Commun Signal 2017 Jun 21;15(1):24. Epub 2017 Jun 21.
    Department of Biology, McMaster University, Hamilton, L8S 4K1, ON, Canada.
    Background: In mammalian intestines, Notch signaling plays a critical role in mediating cell fate decisions; it promotes the absorptive (or enterocyte) cell fate, while concomitantly inhibiting the secretory cell fate (i.e. goblet, Paneth and enteroendocrine cells). Read More

    The role of JAK-STAT signaling pathway and its regulators in the fate of T helper cells.
    Cell Commun Signal 2017 Jun 21;15(1):23. Epub 2017 Jun 21.
    Department of immunology, school of medicine, Iran University of Medical Sciences, Tehran, Iran.
    The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway plays critical roles in orchestrating of immune system, especially cytokine receptors and they can modulate the polarization of T helper cells. This pathway is regulated by an array of regulator proteins, including Suppressors of Cytokine Signaling (SOCS), Protein Inhibitors of Activated STATs (PIAS) and Protein Tyrosine Phosphatases (PTPs) determining the initiation, duration and termination of the signaling cascades. Dysregulation of the JAK-STAT pathway in T helper cells may result in various immune disorders. Read More

    Identification of EGF-NF-κB-FOXC1 signaling axis in basal-like breast cancer.
    Cell Commun Signal 2017 Jun 19;15(1):22. Epub 2017 Jun 19.
    Department of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
    Background: The pathogenesis of human basal-like breast cancer (BLBC) is not well understood and patients with BLBC have a poor prognosis. Expression of the epidermal growth factor receptor (EGFR) and nuclear factor-κB (NF-κB) is well-known to be upregulated in BLBC. The forkhead box C1 (FOXC1) transcription factor, an important prognostic biomarker specific for BLBC, has been shown to be induced by EGF and is critical for EGF effects in breast cancer cells. Read More

    LASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pathway meditated epithelial-mesenchymal transition.
    Cell Commun Signal 2017 Jun 12;15(1):21. Epub 2017 Jun 12.
    Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
    Background: LASP2 (LIM and SH3 Protein 2) is a small focal adhesion protein belongs to nebulin protein family. As the newest member of nebulette family, the function of LASP2 remains to be identified.

    Methods: The relationship between LASP2 expression and clinical characteristics of CRC was analyzed in 89 paraffin-embedded archived CRC specimens by immunohistochemistry (IHC). Read More

    The role of TGF-β and its crosstalk with RAC1/RAC1b signaling in breast and pancreas carcinoma.
    Cell Commun Signal 2017 May 12;15(1):19. Epub 2017 May 12.
    Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Campus Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany.
    This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. Read More

    DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion.
    Cell Commun Signal 2017 May 8;15(1):18. Epub 2017 May 8.
    Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, 1365-C Clifton Road, Clinical Building C3088, Atlanta, GA, 30322, USA.
    Background: Death receptor (DR5), a well-characterized death domain-containing cell surface pro-apoptotic protein, has been suggested to suppress cancer cell invasion and metastasis. However, the underlying mechanisms have not been fully elucidated. Our recent work demonstrates that DR5 suppression promotes cancer cell invasion and metastasis through caspase-8/TRAF2-mediated activation of ERK and JNK signaling and MMP1 elevation. Read More

    Senescence-associated IL-6 and IL-8 cytokines induce a self- and cross-reinforced senescence/inflammatory milieu strengthening tumorigenic capabilities in the MCF-7 breast cancer cell line.
    Cell Commun Signal 2017 May 4;15(1):17. Epub 2017 May 4.
    Cellular and Molecular Physiology Group, Instituto de Investigaciones Biomédicas, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá D.C., 111311, Colombia.
    Background: There is compelling evidence associating senescent cells with the malignant progression of tumours. Of all senescence-related mechanisms, the so-called senescence-associated secretory phenotype (SASP) has attracted much attention. Since the pro-inflammatory cytokines IL-6 and IL-8 are consistently present in the SASP, and secreted by highly aggressive breast cancer cell lines, we aimed at elucidating their role on the less aggressive breast cancer cell line MCF-7, which does not secret these cytokines. Read More

    The role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma (RCC): the crucial role of ARC in the inhibition of extrinsic and intrinsic apoptotic signalling.
    Cell Commun Signal 2017 May 2;15(1):16. Epub 2017 May 2.
    Institute of Pathology, Heinrich Heine University Hospital, Medical Faculty, Moorenstrasse 5, 40225, Düsseldorf, Germany.
    Background: Renal cell carcinomas (RCCs) display broad resistance against conventional radio- and chemotherapies, which is due at least in part to impairments in both extrinsic and intrinsic apoptotic pathways. One important anti-apoptotic factor that is strongly overexpressed in RCCs and known to inhibit both apoptotic pathways is ARC (apoptosis repressor with a CARD domain).

    Methods: Expression and subcellular distribution of ARC in RCC tissue samples and RCC cell lines were determined by immunohistochemistry and fluorescent immunohistochemistry, respectively. Read More

    From inflammation to gastric cancer - the importance of Hedgehog/GLI signaling in Helicobacter pylori-induced chronic inflammatory and neoplastic diseases.
    Cell Commun Signal 2017 Apr 20;15(1):15. Epub 2017 Apr 20.
    Division of Molecular Tumor Biology, Cancer Cluster Salzburg, Department of Molecular Biology, Paris-Lodron University of Salzburg, Hellbrunner Strasse 34, A-5020, Salzburg, Austria.
    Infections with the human pathogen Helicobacter pylori (H. pylori) are closely associated with the development of inflammatory disorders and neoplastic transformation of the gastric epithelium. Drastic changes in the micromilieu involve a complex network of H. Read More

    TGFBR2-dependent alterations of exosomal cargo and functions in DNA mismatch repair-deficient HCT116 colorectal cancer cells.
    Cell Commun Signal 2017 Apr 4;15(1):14. Epub 2017 Apr 4.
    Department of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
    Background: Colorectal cancers (CRCs) that lack DNA mismatch repair function exhibit the microsatellite unstable (MSI) phenotype and are characterized by the accumulation of frameshift mutations at short repetitive DNA sequences (microsatellites). These tumors recurrently show inactivating frameshift mutations in the tumor suppressor Transforming Growth Factor Beta Receptor Type 2 (TGFBR2) thereby abrogating downstream signaling. How altered TGFBR2 signaling affects exosome-mediated communication between MSI tumor cells and their environment has not been resolved. Read More

    The double-edged sword of (re)expression of genes by hypomethylating agents: from viral mimicry to exploitation as priming agents for targeted immune checkpoint modulation.
    Cell Commun Signal 2017 Mar 31;15(1):13. Epub 2017 Mar 31.
    3rd Medical Department with Hematology and Medical Oncology, Hemostaseology, Rheumatology and Infectious Diseases, Laboratory for Immunological and Molecular Cancer Research, Oncologic Center, Paracelsus Medical University Salzburg, Müllner Hauptstraße 48, A-5020, Salzburg, Austria.
    Hypomethylating agents (HMAs) have been widely used over the last decade, approved for use in myelodysplastic syndrome (MDS), chronic myelomonocytic leukemia (CMML) and acute myeloid leukemia (AML). The proposed central mechanism of action of HMAs, is the reversal of aberrant methylation in tumor cells, thus reactivating CpG-island promoters and leading to (re)expression of tumor suppressor genes. Recent investigations into the mode of action of azacitidine (AZA) and decitabine (DAC) have revealed new molecular mechanisms that impinge on tumor immunity via induction of an interferon response, through activation of endogenous retroviral elements (ERVs) that are normally epigenetically silenced. Read More

    Understanding cell signaling in cancer stem cells for targeted therapy - can phosphoproteomics help to reveal the secrets?
    Cell Commun Signal 2017 Mar 29;15(1):12. Epub 2017 Mar 29.
    Department of Molecular Biology, Cancer Cluster Salzburg, Paris-Lodron University of Salzburg, Hellbrunner Strasse 34, 5020, Salzburg, Austria.
    Background: Cancer represents heterogeneous and aberrantly proliferative manifestations composed of (epi)genetically and phenotypically distinct cells with a common clonal origin. Cancer stem cells (CSC) make up a rare subpopulation with the remarkable capacity to initiate, propagate and spread a malignant disease. Furthermore, CSC show increased therapy resistance, thereby contributing to disease relapse. Read More

    Erratum to: Integrin-FAK signaling rapidly and potently promotes mitochondrial function through STAT3.
    Cell Commun Signal 2017 Mar 27;15(1):11. Epub 2017 Mar 27.
    Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Building 178, Maple Ave, PO Box 70582, Johnson City, TN37614, USA.

    c-Met expression and activity in urogenital cancers - novel aspects of signal transduction and medical implications.
    Cell Commun Signal 2017 Feb 17;15(1):10. Epub 2017 Feb 17.
    Institute of Biochemistry II, University Hospital Jena, Nonnenplan 2-4, D-07743, Jena, Germany.
    C-Met is a receptor tyrosine kinase with multiple functions throughout embryonic development, organogenesis and wound healing and is expressed in various epithelia. The ligand of c-Met is Hepatocyte Growth Factor (HGF) which is secreted among others by mesenchymal stroma/stem (MSC) cells.Physiological c-Met functions are centred around processes that underly cellular motility and invasive growth. Read More

    Translationally controlled tumour protein TCTP is induced early in human colorectal tumours and contributes to the resistance of HCT116 colon cancer cells to 5-FU and oxaliplatin.
    Cell Commun Signal 2017 Feb 1;15(1). Epub 2017 Feb 1.
    Illawarra Health and Medical Research Institute (IHMRI), University of Wollongong, Northfields Avenue, Wollongong, NSW, 2522, Australia.
    Background: Translationally controlled tumour protein TCTP is an anti-apoptotic protein frequently overexpressed in cancers, where high levels are often associated with poor patient outcome. TCTP may be involved in protecting cancer cells against the cytotoxic action of anti-cancer drugs. Here we study the early increase of TCTP levels in human colorectal cancer (CRC) and the regulation of TCTP expression in HCT116 colon cancer cells, in response to treatment with the anti-cancer drugs 5-FU and oxaliplatin. Read More

    Acute myeloid leukemia - strategies and challenges for targeting oncogenic Hedgehog/GLI signaling.
    Cell Commun Signal 2017 Jan 25;15(1). Epub 2017 Jan 25.
    Cancer Cluster Salzburg, Salzburg Cancer Research Institute (SCRI) - Laboratory for Immunological and Molecular Cancer Research (LIMCR), 5020, Salzburg, Austria.
    Treatment of acute myeloid leukemia (AML), an aggressive and heterogeneous hematological malignancy, remains a challenge. Despite advances in our understanding of the complex genetics and biology of AML pathophysiology, these findings have been translated to the clinic with only limited success, and poor outcomes persist for the majority of patients. Thus, novel treatment strategies are clearly needed for achieving deeper and prolonged remissions and for avoiding the development of resistance. Read More

    The Id-protein family in developmental and cancer-associated pathways.
    Cell Commun Signal 2017 Jan 25;15(1). Epub 2017 Jan 25.
    Department of Molecular Biology, University of Salzburg, Billrothstrasse 11, Salzburg, 5020, Austria.
    Inhibitors of DNA binding and cell differentiation (Id) proteins are members of the large family of the helix-loop-helix (HLH) transcription factors, but they lack any DNA-binding motif. During development, the Id proteins play a key role in the regulation of cell-cycle progression and cell differentiation by modulating different cell-cycle regulators both by direct and indirect mechanisms. Several Id-protein interacting partners have been identified thus far, which belong to structurally and functionally unrelated families, including, among others, the class I and II bHLH transcription factors, the retinoblastoma protein and related pocket proteins, the paired-box transcription factors, and the S5a subunit of the 26 S proteasome. Read More

    Unraveling the regulation of mTORC2 using logical modeling.
    Cell Commun Signal 2017 Jan 19;15(1). Epub 2017 Jan 19.
    Group for Discrete Biomathematics, Department for Mathematics and Computer Science, Freie Universitaet Berlin, Arnimallee 7, Berlin, 14195, Germany.
    Background: The mammalian target of rapamycin (mTOR) is a regulator of cell proliferation, cell growth and apoptosis working through two distinct complexes: mTORC1 and mTORC2. Although much is known about the activation and inactivation of mTORC1, the processes controlling mTORC2 remain poorly characterized. Experimental and modeling studies have attempted to explain the regulation of mTORC2 but have yielded several conflicting hypotheses. Read More

    Reactivation of dormant anti-tumor immunity - a clinical perspective of therapeutic immune checkpoint modulation.
    Cell Commun Signal 2017 Jan 19;15(1). Epub 2017 Jan 19.
    Third Medical Department with Hematology, Medical Oncology, Hemostaseology, Infectious Disease and Rheumatology, Oncologic Center, Paracelsus Medical University Salzburg, Müllner Hauptstraße 48, A-5020, Salzburg, Austria.
    In favor of their outgrowth, cancer cells must resist immune surveillance and edit the immune response. Cancer immunoediting is characterized by fundamental changes in the cellular composition and the inflammatory cytokine profiles in the microenvironment of the primary tumor and metastatic niches, with an ever increasing complexity of interactions between tumor cells and the immune system. Recent data suggest that genetic instability and immunoediting are not necessarily disparate processes. Read More

    HECTD1 controls the protein level of IQGAP1 to regulate the dynamics of adhesive structures.
    Cell Commun Signal 2017 Jan 5;15(1). Epub 2017 Jan 5.
    Department of Biomedicine, University Hospital, University of Basel, Basel, Switzerland.
    Background: Cell migration including collective cell movement and individual cell migration are crucial factors in embryogenesis. During the spreading/migration of cells, several types of adhesive structures physically interacting with the extracellular matrix (ECM) or with another cell have been described and the formation and maturation of adhesion structures are coordinated, however the molecular pathways involved are still not fully understood.

    Results: We generated a mouse embryonic fibroblast line (MEF) from homozygous mutant (Hectd1 (R/R) , Hectd1 (Gt(RRC200)) ) mouse of the E3 ubiquitin ligase for inhibin B receptor (Hectd1). Read More

    T cell exhaustion: from pathophysiological basics to tumor immunotherapy.
    Cell Commun Signal 2017 Jan 5;15(1). Epub 2017 Jan 5.
    Laboratory for Immunological and Molecular Cancer Research, Department of Internal Medicine III with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Center, Paracelsus Medical University, Müllner Hauptstrasse 48, Salzburg, 5020, Austria.
    The immune system is capable of distinguishing between danger- and non-danger signals, thus inducing either an appropriate immune response against pathogens and cancer or inducing self-tolerance to avoid autoimmunity and immunopathology. One of the mechanisms that have evolved to prevent destruction by the immune system, is to functionally silence effector T cells, termed T cell exhaustion, which is also exploited by viruses and cancers for immune escape In this review, we discuss some of the phenotypic markers associated with T cell exhaustion and we summarize current strategies to reinvigorate exhausted T cells by blocking these surface marker using monoclonal antibodies. Read More

    Bacterial serine protease HtrA as a promising new target for antimicrobial therapy?
    Cell Commun Signal 2017 Jan 10;15(1). Epub 2017 Jan 10.
    Division of Microbiology, University of Erlangen-Nuremberg, Staudtstr. 5, D-91058, Erlangen, Germany.
    Recent studies have demonstrated that the bacterial chaperone and serine protease high temperature requirement A (HtrA) is closely associated with the establishment and progression of several infectious diseases. HtrA activity enhances bacterial survival under stress conditions, but also has direct effects on functions of the cell adhesion protein E-cadherin and extracellular matrix proteins, including fibronectin and proteoglycans. Although HtrA cannot be considered as a pathogenic factor per se, it exhibits favorable characteristics making HtrA a potentially attractive drug target to combat various bacterial infections. Read More

    Aldose reductase mediates endothelial cell dysfunction induced by high uric acid concentrations.
    Cell Commun Signal 2017 Jan 5;15(1). Epub 2017 Jan 5.
    Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Beijing, 100853, People's Republic of China.
    Background: Uric acid (UA) is an antioxidant found in human serum. However, high UA levels may also have pro-oxidant functions. According to previous research, aldose reductase (AR) plays a vital role in the oxidative stress-related complications of diabetes. Read More

    Integrin-FAK signaling rapidly and potently promotes mitochondrial function through STAT3.
    Cell Commun Signal 2016 12 15;14(1):32. Epub 2016 Dec 15.
    Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Building 178, Maple Ave, PO Box 70582, Johnson City, TN37614, USA.
    Background: STAT3 is increasingly becoming known for its non-transcriptional regulation of mitochondrial bioenergetic function upon activation of its S727 residue (S727-STAT3). Lengthy mitochondrial dysfunction can lead to cell death. We tested whether an integrin-FAK-STAT3 signaling pathway we recently discovered regulates mitochondrial function and cell survival, and treatments thereof. Read More

    Attenuation of chemokine receptor function and surface expression as an immunomodulatory strategy employed by human cytomegalovirus is linked to vGPCR US28.
    Cell Commun Signal 2016 12 12;14(1):31. Epub 2016 Dec 12.
    Department of Chemistry and Pharmacy, Emil Fischer Center, University of Erlangen-Nuremberg, Erlangen, Germany.
    Background: Some herpesviruses like human cytomegalovirus (HCMV) encode viral G protein-coupled receptors that cause reprogramming of cell signaling to facilitate dissemination of the virus, prevent immune surveillance and establish life-long latency. Human GPCRs are known to function in complex signaling networks involving direct physical interactions as well as indirect crosstalk of orthogonal signaling networks. The human chemokine receptor CXCR4 is expressed on hematopoietic stem cells, leukocytes, endothelial and epithelial cells, which are infected by HCMV or display reservoirs of latency. Read More

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