Critical Role of AMPK/FoxO3A Axis in Globular Adiponectin-Induced Cell Cycle Arrest and Apoptosis in Cancer Cells

2015 ◽  
Vol 231 (2) ◽  
pp. 357-369 ◽  
Author(s):  
Anup Shrestha ◽  
Saroj Nepal ◽  
Mi Jin Kim ◽  
Jae Hoon Chang ◽  
Sang-Hyun Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Critical Role ◽  
Cycle Arrest ◽  
Globular Adiponectin ◽  
Apoptosis In Cancer Cells

Novel small molecule inhibitor of Kpnβ1 induces cell cycle arrest and apoptosis in cancer cells

2021 ◽  
pp. 112637
Author(s):  
Aderonke Ajayi-Smith ◽  
Pauline van der Watt ◽  
Nonkululeko Mkwanazi ◽  
Sarah Carden ◽  
John O. Trent ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Small Molecule ◽  
Small Molecule Inhibitor ◽  
Cycle Arrest ◽  
Molecule Inhibitor ◽  
Apoptosis In Cancer Cells

scholarly journals Critical role of PP2A-B56 family protein degradation in HIV-1 Vif mediated G2 cell cycle arrest

2020 ◽  
Vol 527 (1) ◽  
pp. 257-263
Author(s):  
Kayoko Nagata ◽  
Keisuke Shindo ◽  
Yusuke Matsui ◽  
Kotaro Shirakawa ◽  
Akifumi Takaori-Kondo
Keyword(s):  
Cell Cycle ◽  
Protein Degradation ◽  
Cell Cycle Arrest ◽  
Critical Role ◽  
Cycle Arrest ◽  
Family Protein ◽  
G2 Cell Cycle Arrest ◽  
Hiv 1

scholarly journals N-Myristoyltransferase Inhibition Induces ER-Stress, Cell Cycle Arrest, and Apoptosis in Cancer Cells

2016 ◽  
Vol 11 (8) ◽  
pp. 2165-2176 ◽  
Author(s):  
Emmanuelle Thinon ◽  
Julia Morales-Sanfrutos ◽  
David J. Mann ◽  
Edward W. Tate
Keyword(s):  
Cell Cycle ◽  
Er Stress ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cycle Arrest ◽  
Apoptosis In Cancer Cells

scholarly journals The role of MAP kinase in TPA-mediated cell cycle arrest of human breast cancer cells

Oncogene ◽  
1998 ◽  
Vol 16 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Jacqueline Alblas ◽  
Rivka Slager-Davidov ◽  
Paul H Steenbergh ◽  
John S Sussenbach ◽  
Bart van der Burg
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cycle Arrest

scholarly journals Piper nigrum ethanolic extract rich in piperamides causes ROS overproduction, oxidative damage in DNA leading to cell cycle arrest and apoptosis in cancer cells

2016 ◽  
Vol 189 ◽  
pp. 139-147 ◽  
Author(s):  
Valdelúcia Maria Alves de Souza Grinevicius ◽  
Maicon Roberto Kviecinski ◽  
Nádia Sandrini Ramos Santos Mota ◽  
Fabiana Ourique ◽  
Luiza Sheyla Evenni Porfirio Will Castro ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oxidative Damage ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Ethanolic Extract ◽  
Piper Nigrum ◽  
Cycle Arrest ◽  
Apoptosis In Cancer Cells

scholarly journals Nuclear Translocation of Glutaminase GLS2 in Human Cancer Cells Associates with Proliferation Arrest and Differentiation

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Amada R. López de la Oliva ◽  
José A. Campos-Sandoval ◽  
María C. Gómez-García ◽  
Carolina Cardona ◽  
Mercedes Martín-Rufián ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Cancer ◽  
Metabolic Reprogramming ◽  
Nuclear Targeting ◽  
Human Cancer Cells ◽  
Cycle Arrest

AbstractGlutaminase (GA) catalyzes the first step in mitochondrial glutaminolysis playing a key role in cancer metabolic reprogramming. Humans express two types of GA isoforms: GLS and GLS2. GLS isozymes have been consistently related to cell proliferation, but the role of GLS2 in cancer remains poorly understood. GLS2 is repressed in many tumor cells and a better understanding of its function in tumorigenesis may further the development of new therapeutic approaches. We analyzed GLS2 expression in HCC, GBM and neuroblastoma cells, as well as in monkey COS-7 cells. We studied GLS2 expression after induction of differentiation with phorbol ester (PMA) and transduction with the full-length cDNA of GLS2. In parallel, we investigated cell cycle progression and levels of p53, p21 and c-Myc proteins. Using the baculovirus system, human GLS2 protein was overexpressed, purified and analyzed for posttranslational modifications employing a proteomics LC-MS/MS platform. We have demonstrated a dual targeting of GLS2 in human cancer cells. Immunocytochemistry and subcellular fractionation gave consistent results demonstrating nuclear and mitochondrial locations, with the latter being predominant. Nuclear targeting was confirmed in cancer cells overexpressing c-Myc- and GFP-tagged GLS2 proteins. We assessed the subnuclear location finding a widespread distribution of GLS2 in the nucleoplasm without clear overlapping with specific nuclear substructures. GLS2 expression and nuclear accrual notably increased by treatment of SH-SY5Y cells with PMA and it correlated with cell cycle arrest at G2/M, upregulation of tumor suppressor p53 and p21 protein. A similar response was obtained by overexpression of GLS2 in T98G glioma cells, including downregulation of oncogene c-Myc. Furthermore, human GLS2 was identified as being hypusinated by MS analysis, a posttranslational modification which may be relevant for its nuclear targeting and/or function. Our studies provide evidence for a tumor suppressor role of GLS2 in certain types of cancer. The data imply that GLS2 can be regarded as a highly mobile and multilocalizing protein translocated to both mitochondria and nuclei. Upregulation of GLS2 in cancer cells induced an antiproliferative response with cell cycle arrest at the G2/M phase.

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