328 results match your criteria bcl2l1 mcl1


Luteolin inhibits proliferation, triggers apoptosis and modulates Akt/mTOR and MAP kinase pathways in HeLa cells.

Oncol Lett 2021 Mar 7;21(3):192. Epub 2021 Jan 7.

School of Life Sciences, Manipal Academy of Higher Education, Dubai, United Arab Emirates.

Flavonoids, a subclass of polyphenols, have been shown to be effective against several types of cancer, by decreasing proliferation and inducing apoptosis. Therefore, the aim of the present study was to assess the anti-carcinogenic potential of luteolin on HeLa human cervical cancer cells, through the use of a cell viability assay, DNA fragmentation assay, mitochondrial membrane potential assay, cell cycle analysis using Annexin/PI staining and flow cytometry, gene expression analysis and a protein profiling array. Luteolin treatment exhibited cytotoxicity towards HeLa cells in a dose- and time-dependent manner, and its anti-proliferative properties were confirmed by accumulation of luteolin-treated cells in sub-G phases. Read More

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Identification of a Dexamethasone Mediated Radioprotection Mechanism Reveals New Therapeutic Vulnerabilities in Glioblastoma.

Cancers (Basel) 2021 Jan 19;13(2). Epub 2021 Jan 19.

Cancer Signalling Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), 31008 Pamplona, Spain.

(1) Background: Despite the indisputable effectiveness of dexamethasone (DEXA) to reduce inflammation in glioblastoma (GBM) patients, its influence on tumour progression and radiotherapy response remains controversial. (2) Methods: We analysed patient data and used expression and cell biological analyses to assess effects of DEXA on GBM cells. We tested the efficacy of tyrosine kinase inhibitors in vitro and in vivo. Read More

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January 2021

The role of alternative splicing in cancer: From oncogenesis to drug resistance.

Drug Resist Updat 2020 12 28;53:100728. Epub 2020 Sep 28.

Department of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, Amsterdam, Netherlands. Electronic address:

Alternative splicing is a tightly regulated process whereby non-coding sequences of pre-mRNA are removed and protein-coding segments are assembled in diverse combinations, ultimately giving rise to proteins with distinct or even opposing functions. In the past decade, whole genome/transcriptome sequencing studies revealed the high complexity of splicing regulation, which occurs co-transcriptionally and is influenced by chromatin status and mRNA modifications. Consequently, splicing profiles of both healthy and malignant cells display high diversity and alternative splicing was shown to be widely deregulated in multiple cancer types. Read More

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December 2020

GSK3β suppression inhibits MCL1 protein synthesis in human acute myeloid leukemia cells.

J Cell Physiol 2021 Jan 22;236(1):570-586. Epub 2020 Jun 22.

Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.

Previous studies have shown that glycogen synthase kinase 3β (GSK3β) suppression is a potential strategy for human acute myeloid leukemia (AML) therapy. However, the cytotoxic mechanism associated with GSK3β suppression remains unresolved. Thus, the underlying mechanism of N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea (AR-A014418)-elicited GSK3β suppression in the induction of AML U937 and HL-60 cell death was investigated in this study. Read More

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January 2021

Albendazole-Induced SIRT3 Upregulation Protects Human Leukemia K562 Cells from the Cytotoxicity of MCL1 Suppression.

Int J Mol Sci 2020 May 30;21(11). Epub 2020 May 30.

Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.

Previous studies have shown that MCL1 stabilization confers cancer cells resistance to microtubule targeting agents (MTAs) and functionally extends the lifespan of MTA-triggered mitotically arrested cells. Albendazole (ABZ), a benzimidazole anthelmintic, shows microtubule-destabilizing activity and has been repositioned for cancer therapies. To clarify the role of MCL1 in ABZ-induced apoptosis, we investigated the cytotoxicity of ABZ on human leukemia K562 cells. Read More

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Pericyte-myofibroblast transition in the human lung.

Biochem Biophys Res Commun 2020 07 27;528(2):269-275. Epub 2020 May 27.

Department of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan. Electronic address:

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease that includes fibroblastic foci (FF). It has been increasingly appreciated that the origin of collagen-overproducing cells such as pathological myofibroblasts in FF is pericytes. However, neither pericytes derived from the lung nor FF in the IPF lung have not been fully characterized. Read More

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Separase-triggered apoptosis enforces minimal length of mitosis.

Nature 2020 04 8;580(7804):542-547. Epub 2020 Apr 8.

Chair of Genetics, University of Bayreuth, Bayreuth, Germany.

Prolonged mitosis often results in apoptosis. Shortened mitosis causes tumorigenic aneuploidy, but it is unclear whether it also activates the apoptotic machinery. Separase, a cysteine protease and trigger of all eukaryotic anaphases, has a caspase-like catalytic domain but has not previously been associated with cell death. Read More

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Noncanonical Cell Fate Regulation by Bcl-2 Proteins.

Trends Cell Biol 2020 07 16;30(7):537-555. Epub 2020 Apr 16.

Université de Paris, Paris, France; Department of Physiology, YLL School of Medicine and NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore; National University Cancer Institute, National University Health System, Singapore. Electronic address:

Bcl-2 proteins are widely known as key controllers of mitochondrial outer membrane permeabilization, arguably the most important step of intrinsic apoptosis. Accumulating evidence indicate that most, if not all, members of the Bcl-2 protein family also mediate a number of apoptosis-unrelated functions. Intriguingly, many of these functions ultimately impinge on cell fate decisions via apoptosis-dependent or -independent mechanisms, delineating a complex network through which Bcl-2 family members regulate cell survival and death. Read More

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BCL-2 Proteins in Pathogenesis and Therapy of B-Cell Non-Hodgkin Lymphomas.

Cancers (Basel) 2020 Apr 10;12(4). Epub 2020 Apr 10.

Institute of Pathological Physiology, First Faculty of Medicine, Charles University in Prague, 12853 Prague, Czech Republic.

The ability to inhibit mitochondrial apoptosis is a hallmark of B-cell non-Hodgkin lymphomas (B-NHL). Activation of mitochondrial apoptosis is tightly controlled by members of B-cell leukemia/lymphoma-2 (BCL-2) family proteins via protein-protein interactions. Altering the balance between anti-apoptotic and pro-apoptotic BCL-2 proteins leads to apoptosis evasion and extended survival of malignant cells. Read More

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A direct comparison of selective BH3-mimetics reveals BCL-X, BCL-2 and MCL-1 as promising therapeutic targets in neuroblastoma.

Br J Cancer 2020 05 18;122(10):1544-1551. Epub 2020 Mar 18.

Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Frankfurt, Germany.

Background: Despite advances in the treatment of neuroblastoma, patients with high-risk disease still have dismal survival prognosis. Neuroblastoma cells display elevated expression of the antiapoptotic BCL-2 proteins, suggesting that BH3-mimetics may be a promising treatment option. Here, we investigated the role of BCL-2, BCL-X and MCL-1 in neuroblastoma. Read More

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MCL1 Is Required for Maintenance of Intestinal Homeostasis and Prevention of Carcinogenesis in Mice.

Gastroenterology 2020 07 14;159(1):183-199. Epub 2020 Mar 14.

Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland. Electronic address:

Background & Aims: Intestinal epithelial homeostasis depends on a tightly regulated balance between intestinal epithelial cell (IEC) death and proliferation. While the disruption of several IEC death regulating factors result in intestinal inflammation, the loss of the anti-apoptotic BCL2 family members BCL2 and BCL2L1 has no effect on intestinal homeostasis in mice. We investigated the functions of the antiapoptotic protein MCL1, another member of the BCL2 family, in intestinal homeostasis in mice. Read More

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Co-inhibition of BET proteins and PI3Kα triggers mitochondrial apoptosis in rhabdomyosarcoma cells.

Oncogene 2020 05 11;39(19):3837-3852. Epub 2020 Mar 11.

Institute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.

Remodeling transcription by targeting bromodomain and extraterminal (BET) proteins has emerged as promising anticancer strategy. Here, we identify a novel synergistic interaction of the BET inhibitor JQ1 with the PI3Kα-specific inhibitor BYL719 to trigger mitochondrial apoptosis and to suppress tumor growth in models of rhabdomyosarcoma (RMS). RNA-Seq revealed that JQ1/BYL719 co-treatment shifts the overall balance of BCL-2 family gene expression towards apoptosis and upregulates expression of BMF, BCL2L11 (BIM), and PMAIP1 (NOXA) while downregulating BCL2L1 (BCL-x). Read More

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MCL1 inhibition is effective against a subset of small-cell lung cancer with high MCL1 and low BCL-X expression.

Cell Death Dis 2020 03 9;11(3):177. Epub 2020 Mar 9.

Department of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.

There have been few advances in the treatment of small-cell lung cancer (SCLC) because of the lack of targets. MCL1, a member of the anti-apoptotic BCL-2 family, may be a treatment target in several cancers, including SCLC. However, whether the expression profile of the anti-apoptotic BCL-2 family affects MCL1 inhibition strategy is unknown. Read More

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Targeting BCL-2 proteins in pediatric cancer: Dual inhibition of BCL-X and MCL-1 leads to rapid induction of intrinsic apoptosis.

Cancer Lett 2020 07 4;482:19-32. Epub 2020 Mar 4.

Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Komturstr. 3a, 60528, Frankfurt, Germany; German Cancer Consortium (DKTK), Partner site Frankfurt, Germany; German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address:

With the development of potent and selective inhibitors of MCL-1 (S63845) and BCL-X (A-1331852) novel cancer treatment options have emerged. BCL-2 family proteins are important regulators of apoptosis in pediatric solid tumors. In the current study, we discover that rhabdomyosarcoma, Ewing sarcoma, osteosarcoma and neuroblastoma cell lines are co-dependent on BCL-X and MCL-1 for survival. Read More

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Venetoclax, bortezomib and S63845, an MCL1 inhibitor, in multiple myeloma.

J Pharm Pharmacol 2020 May 17;72(5):728-737. Epub 2020 Feb 17.

Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam, Hong Kong.

Objectives: Venetoclax, an orally available BCL2-selective inhibitor, has demonstrated promising single-agent anti-tumour activity in myeloma especially patients with t(11;14). Herein, whether venetoclax sensitivity could be enhanced or restored in combination with bortezomib or S63845, a novel MCL1-selective inhibitor, was examined in human myeloma cell lines (HMCLs), including bortezomib-resistant HMCLs.

Methods: By MTS assay, half-maximal inhibitory concentration (IC ) and hence sensitivity/resistance to venetoclax, bortezomib and S63845 were determined. Read More

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Genetic screens in isogenic mammalian cell lines without single cell cloning.

Nat Commun 2020 02 6;11(1):752. Epub 2020 Feb 6.

Genetic Perturbation Platform, Broad Institute of MIT and Harvard, 75 Ames Street, Cambridge, MA, 02142, USA.

Isogenic pairs of cell lines, which differ by a single genetic modification, are powerful tools for understanding gene function. Generating such pairs of mammalian cells, however, is labor-intensive, time-consuming, and, in some cell types, essentially impossible. Here, we present an approach to create isogenic pairs of cells that avoids single cell cloning, and screen these pairs with genome-wide CRISPR-Cas9 libraries to generate genetic interaction maps. Read More

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February 2020

Apoptosis signaling molecules as treatment targets in head and neck squamous cell carcinoma.

Laryngoscope 2020 11 2;130(11):2643-2649. Epub 2020 Jan 2.

Department of Biochemistry, Department of Medicine, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York, U.S.A.

Objectives: To evaluate BCL-2 family signaling molecules in head and neck squamous cell carcinoma (HNSCC) and examine the ability of therapeutic agents with variable mechanisms of action to induce apoptosis in HNSCC cells.

Methods: messenger ribonculeic acid (mRNA) expression of BAK, BAX, B-cell lymphoma (Bcl-2), BCL2 Like 1 (BCL2L1), and MCL1 were measured in The Cancer Genome Atlas (TCGA) head and neck cancer dataset, as well as in a dataset from a cohort at Montefiore Medical Center (MMC). Protein expression was similarly evaluated in a panel of HNSCC cell lines (HN30, HN31, HN5, MDA686LN, UMSCC47). Read More

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November 2020

Heterogeneous Pattern of Dependence on Anti-Apoptotic BCL-2 Family Proteins upon CHOP Treatment in Diffuse Large B-Cell Lymphoma.

Int J Mol Sci 2019 Nov 30;20(23). Epub 2019 Nov 30.

Department of Hematology, University Medical Center Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.

Expression of the anti-apoptotic B-cell lymphoma 2 (BCL-2) protein in patients with diffuse large B-cell lymphoma (DLBCL) strongly correlates with resistance to standard therapy with cyclophosphamide, vincristine, doxorubicin, prednisolone, and rituximab (R-CHOP). Although studies focus mainly on the contribution of BCL-2, here we also investigate the contribution of other anti-apoptotic proteins to CHOP-therapy resistance in DLBCL. Functional dynamic BCL-2 homology (BH)3 profiling was applied to DLBCL cell lines upon CHOP treatment or single CHOP compounds. Read More

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November 2019

Potent efficacy of MCL-1 inhibitor-based therapies in preclinical models of mantle cell lymphoma.

Oncogene 2020 02 26;39(9):2009-2023. Epub 2019 Nov 26.

Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Melbourne, Victoria, 3052, Australia.

Apoptosis-regulating BCL-2 family members, which can promote malignant transformation and resistance to therapy, have become prime therapeutic targets, as illustrated by the striking efficacy in certain lymphoid malignancies of the BCL-2-specific inhibitor venetoclax. In other lymphoid malignancies, however, such as the aggressive mantle cell lymphoma (MCL), cell survival might rely instead or also on BCL-2 relative MCL-1. We have explored MCL-1 as a target for killing MCL cells by both genetic and pharmacologic approaches. Read More

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February 2020

Inhibiting the expression of anti-apoptotic genes BCL2L1 and MCL1, and apoptosis induction in glioblastoma cells by microRNA-342.

Biomed Pharmacother 2020 Jan 18;121:109641. Epub 2019 Nov 18.

Laboratory for Stem Cell & Regenerative Medicine, Natural and Medicinal Sciences Research Center, University of Nizwa, Nizwa, P. O. Box: 33, PC 616, Oman.

Glioma is an aggressive and lethal type of brain tumor that originates from glial cells. Glioblastoma cells confer considerable resistance to induction of apoptosis, which may be due to overexpression of anti-apoptotic proteins, or the reduction of the level of some pro-apoptotic proteins. MicroRNAs (miRNAs) can affect the cell biology pathways, including replication, autophagy, necrosis, and apoptosis by regulating gene expression. Read More

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January 2020

Targeting melanoma's MCL1 bias unleashes the apoptotic potential of BRAF and ERK1/2 pathway inhibitors.

Nat Commun 2019 11 14;10(1):5167. Epub 2019 Nov 14.

Signalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.

BRAF and MEK1/2 inhibitors are effective in melanoma but resistance inevitably develops. Despite increasing the abundance of pro-apoptotic BIM and BMF, ERK1/2 pathway inhibition is predominantly cytostatic, reflecting residual pro-survival BCL2 family activity. Here, we show that uniquely low BCL-X expression in melanoma biases the pro-survival pool towards MCL1. Read More

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November 2019

PROTAC induced-BET protein degradation exhibits potent anti-osteosarcoma activity by triggering apoptosis.

Cell Death Dis 2019 10 25;10(11):815. Epub 2019 Oct 25.

Department of Orthopaedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Targeting oncogenic proteins for degradation using proteolysis-targeting chimera (PROTAC) recently has drawn increasing attention in the field of cancer research. Bromodomain and extra-terminal (BET) family proteins are newly identified cancer-related epigenetic regulators, which have a role in the pathogenesis and progression of osteosarcoma. In this study, we investigated the in vitro and in vivo anti-osteosarcoma activity by targeting BET with a PROTAC molecule BETd-260. Read More

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October 2019

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9.

Artif Cells Nanomed Biotechnol 2019 Dec;47(1):3904-3912

Department of Pharmacy, Zhongshan City People's Hospital , Zhongshan , PR China.

This study aimed to investigate the effect of Junduqing extractive on proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma (NPC) cells and the involved mechanism. Junduqing extractive was prepared. CCK-8 assay found that IC50 of Junduqing extractive in HNE-1 cells was 2. Read More

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December 2019

BH3-only proteins target BCL-xL/MCL-1, not BAX/BAK, to initiate apoptosis.

Cell Res 2019 Nov 24;29(11):942-952. Epub 2019 Sep 24.

Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68198-7696, USA.

It has been widely accepted that mitochondria-dependent apoptosis initiates when select BH3-only proteins (BID, BIM, etc.) directly engage and allosterically activate effector proteins BAX/BAK. Here, through reconstitution of cells lacking all eight pro-apoptotic BH3-only proteins, we demonstrate that all BH3-only proteins primarily target the anti-apoptotic BCL-2 proteins BCL-xL/MCL-1, whose simultaneous suppression enables membrane-mediated spontaneous activation of BAX/BAK. Read More

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November 2019

Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer.

Mol Cancer Res 2019 11 28;17(11):2281-2293. Epub 2019 Aug 28.

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.

High-grade serous ovarian cancer (HGSOC) is often sensitive to initial treatment with platinum and taxane combination chemotherapy, but most patients relapse with chemotherapy-resistant disease. To systematically identify genes modulating chemotherapy response, we performed pooled functional genomic screens in HGSOC cell lines treated with cisplatin, paclitaxel, or cisplatin plus paclitaxel. Genes in the intrinsic pathway of apoptosis were among the top candidate resistance genes in both gain-of-function and loss-of-function screens. Read More

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November 2019

CDK7 inhibitor THZ1 inhibits MCL1 synthesis and drives cholangiocarcinoma apoptosis in combination with BCL2/BCL-XL inhibitor ABT-263.

Cell Death Dis 2019 08 9;10(8):602. Epub 2019 Aug 9.

Department of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, Jiangsu, China.

Cholangiocarcinoma (CCA) is a fatal disease without effective targeted therapy. We screened a small-molecule library of 116 inhibitors targeting different targets of the cell cycle and discovered several kinases, including Cyclin-dependent kinase 7 (CDK7) as vulnerabilities in CCA. Analysis of multiple CCA data sets demonstrated that CDK7 was overexpressed in CCA tissues. Read More

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Thymic Stromal Lymphopoietin Interferes with the Apoptosis of Human Skin Mast Cells by a Dual Strategy Involving STAT5/Mcl-1 and JNK/Bcl-x.

Cells 2019 08 5;8(8). Epub 2019 Aug 5.

Department of Dermatology, Venerology and Allergy, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.

Mast cells (MCs) play critical roles in allergic and inflammatory reactions and contribute to multiple pathologies in the skin, in which they show increased numbers, which frequently correlates with severity. It remains ill-defined how MC accumulation is established by the cutaneous microenvironment, in part because research on human MCs rarely employs MCs matured in the tissue, and extrapolations from other MC subsets have limitations, considering the high level of MC heterogeneity. Thymic stromal lymphopoietin (TSLP)-released by epithelial cells, like keratinocytes, following disturbed homeostasis and inflammation-has attracted much attention, but its impact on skin MCs remains undefined, despite the vast expression of the TSLP receptor by these cells. Read More

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The Covalent CDK7 Inhibitor THZ1 Potently Induces Apoptosis in Multiple Myeloma Cells and .

Clin Cancer Res 2019 10 29;25(20):6195-6205. Epub 2019 Jul 29.

Division of Hematology/Oncology and Palliative Care, Virginia Commonwealth University, Richmond, Virginia.

Purpose: The goal of this study was to characterize the activity of the covalent CDK7 inhibitor THZ1 in multiple myeloma models.

Experimental Design: Multiple myeloma lines were exposed to varying THZ1 concentrations alone or with carfilzomib or ABT-199, after which apoptosis was monitored by flow cytometry, protein expression by Western blot analysis, mRNA by RT-PCR. Analogous studies were performed in cells ectopically expressing c-MYC, MCL-1, or BCL-XL, or CRISPER-Cas CDK7 sgRNA knockout. Read More

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October 2019

Phytosterols and triterpenes from Benth () as potential inhibitors of anti-apoptotic BCL-XL, BCL-2, and MCL-1: an in-silico study.

J Recept Signal Transduct Res 2019 Feb 19;39(1):87-97. Epub 2019 Jun 19.

b Department of Biochemistry, Faculty of Life Sciences , University of Ilorin , Ilorin , Nigeria.

Deregulation of the normal cellular apoptotic function is a fundamental element in the etiology of most cancers and the anti-apoptotic B cell lymphoma 2 (BCL‑2) protein family is known to play crucial role in the regulation of this function. Overexpression of this protein family has been implicated in some cancers, such that agents that could inhibit their over-activity are now being explored for anticancer drug development. A number of studies have revealed the anticancer potential of -derived extracts and compounds. Read More

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February 2019

MCL1 inhibition enhances the therapeutic effect of MEK inhibitors in KRAS-mutant lung adenocarcinoma cells.

Lung Cancer 2019 07 14;133:88-95. Epub 2019 May 14.

Department of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, South 1, West 17, Chuo-ku, Sapporo 060-8556, Japan. Electronic address:

Objectives: MCL1 is an anti-apoptotic BCL2 family member that is highly expressed in various malignant tumors. However, little is known about the role of MCL1 in KRAS-mutant lung adenocarcinomas. In this study, we aimed to clarify whether MCL1 could be a therapeutic target in KRAS-mutant lung adenocarcinomas for which no effective molecular targeted drugs are available. Read More

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