Cyclin D1 controls G1-associated processes, including G0-to-G1 and G1-to-S transitions. This study demonstrates a novel aspect of cyclin D1 as a regulator of the transition between G1 and G0. Overexpression of cyclin D1 in MCF7 breast tumor cells resulted in a continued proliferation under low-serum conditions, whereas nonoverexpressing cells ceased to grow. This difference in growth was due to a reduced exit from G1 to G0 in cyclin D1-overexpressing cells. Our data therefore suggest a model in which cyclin D1 overexpression in tumor cells is responsible for hyperproliferation under growth factor-deprived conditions.
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http://dx.doi.org/10.1128/MCB.16.6.2554 | DOI Listing |
J Biol Chem
January 2025
Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA; Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio, USA. Electronic address:
Selective inhibitors that target cyclin dependent kinases 4 and 6 (CDK4/6i) are FDA approved for treatment of a subset of breast cancers and are being evaluated in numerous clinical trials for other cancers. Despite this advance, a subset of tumors are intrinsically resistant to these drugs and acquired resistance is nearly inevitable. Recent mechanistic evidence suggests that in addition to stalling the cell cycle, the anti-tumor effects of CDK4/6i involve the induction of chromosomal instability (CIN).
View Article and Find Full Text PDFNat Cell Biol
January 2025
CNRS UMR144 - UMR3664, Institut Curie, Sorbonne Université, PSL Research University, Paris, France.
Errors during cell division lead to aneuploidy, which is associated with genomic instability and cell transformation. In response to aneuploidy, cells activate the tumour suppressor p53 to elicit a surveillance mechanism that halts proliferation and promotes senescence. The molecular sensors that trigger this checkpoint are unclear.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
AT-31 BIO Inc., 403 Business Incubation Center, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of Korea; Laboratory of Immunobiology, School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of Korea. Electronic address:
Recombinant GH16B β-agarase-catalyzed liquefaction of 5-7 %(w/v) melted agarose at 50 °C completely hydrolyzed agarose into neoagarohexaose (NA6) and neoagarotetraose (NA4). Subsequent saccharification by recombinant GH50A β-agarase or recombinant GH50A β-agarase/recombinant GH117A α-neoagarobiose hydrolase at 35 °C converted NA6/NA4 into neoagarobiose (NA2) or 3,6-anhydro-L-galactose (L-AHG)/D-galactose, respectively. Purification of NA6/NA4 and NA2 was achieved by Sephadex G-15 column chromatography, while L-AHG was purified by Sephadex G-10, achieving ≥ 98 % purity.
View Article and Find Full Text PDFCell Div
December 2024
Institute for Research in Immunology and Cancer, Département de biochimie et médecine moléculaire, Université de Montréal, Montreal, Québec, Canada.
Background: Mitosis and cytokinesis are regulated by reversible phosphorylation events controlled by kinases and phosphatases. Drosophila Polo kinase, like its human ortholog PLK1, plays several roles in this process. Multiple mechanisms contribute to regulate Polo/PLK1 activity, localization and interactions.
View Article and Find Full Text PDFMethods Mol Biol
November 2024
Faculty of Medicine, Department of Medicine I, Medical Center, University of Freiburg, Freiburg, Germany.
In order to sustain genomic stability by correct DNA replication and mitosis and thus avoid malignant transformation of cells, the cell cycle is a strictly regulated process. Aberrant cell cycle regulation and defects in mitosis in malignant cells are targets of various cancer therapies. Cancer cells may survive antimitotic treatment due to mitotic slippage with a residual activity of the ubiquitin ligase anaphase-promoting complex (APC/C) and a continuous slow ubiquitin-proteasome-dependent cyclin B-degradation leading to mitotic exit.
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