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| http://dx.doi.org/10.1038/s41419-020-2676-9 | DOI Listing |
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Tipping the balance of cell death: alternative splicing as a source of MCL-1S in cancer.
Cell Death Dis
December 2024
Department of Molecular Biology of Cancer, Medical University of Lodz, 6/8 Mazowiecka Street, 92-215, Lodz, Poland.
Apoptosis-regulating proteins from the B-cell lymphoma-2 (BCL-2) family are of continued interest as they represent promising targets for anti-cancer therapies. Myeloid cell leukemia-1 (MCL-1), which usually refers to the long isoform (MCL-1L) is frequently overexpressed in various types of cancer. However, MCL1 pre-mRNA can also undergo alternative splicing through exon skipping to yield the short isoform, MCL-1S.
View Article and Find Full Text PDFHeme promotes venetoclax resistance in multiple myeloma through MEK-ERK signaling and purine biosynthesis.
Blood
December 2024
Winship Cancer Institute, Emory University, Atlanta, Georgia, United States.
We previously demonstrated that reduced intrinsic electron transport chain (ETC) activity predicts and promotes sensitivity to the BCL-2 antagonist, venetoclax (Ven) in multiple myeloma (MM). Heme, an iron-containing prosthetic group, and metabolite is fundamental to maintaining ETC activity. Interrogation of the CD2 subgroup of MM from the CoMMpass trial (NCT01454297), which can be used as a proxy for Ven-sensitive MM (VS MM), shows reduced expression of the conserved heme biosynthesis pathway gene signature.
View Article and Find Full Text PDFProtein Kinase C-β Inhibition and Survival Signaling after Simulated Cardioplegic Ischemia/Reperfusion in Non-Diabetic and Diabetic Human Coronary Arterial Endothelial Cells.
J Am Coll Surg
December 2024
Division of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Rhode Island Hospital, 2 Dudley Street, MOC 360. Providence RI 02905.
Background: Cardioplegic ischemia/reperfusion (I/R) injury poses substantial challenges during postoperative recovery, with diabetic patients particularly susceptible to adverse events. Using a model entailing the subjection of human coronary artery endothelial cells (HCAECs) to simulated cardioplegic I/R, we investigated the potential of protein kinase c β (PKC-β) inhibition to augment cellular survival in this context.
Study Design: HCAECs were isolated from harvested coronary arteries of diabetic (D) and nondiabetic (C) patients (N = 4 per group).
Acid ceramidase controls proteasome inhibitor resistance and is a novel therapeutic target for the treatment of relapsed / refractory multiple myeloma.
Haematologica
December 2024
Department of Tumor Metastasis and Microenvironment., H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612.
Multiple myeloma (MM) patients are often refractory to targeted therapies including proteasome inhibitors (PIs). Here, analysis of RNA sequencing data derived from 672 patients with newly diagnosed or relapsed/refractory disease identified the acid ceramidase, ASAH1, as a key regulator of PI resistance. Genetic or pharmacological blockade of ASAH1 remarkably restored PI sensitivity and protected mice from resistant MM progression in vivo.
View Article and Find Full Text PDFHRK downregulation and augmented BCL-xL binding to BAK confer apoptotic protection to therapy-induced senescent melanoma cells.
Cell Death Differ
December 2024
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Senescent cells are commonly detected in tumors after chemo and radiotherapy, leading to a characteristic cellular phenotype that resists apoptotic cell death. In this study, we used multiple melanoma cell lines, molecular markers, and therapies to investigate the key role of the BCL-2 family proteins in the survival of senescent cells. We first used BH3 profiling to assess changes in apoptotic priming upon senescence induction.
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