Under study was the kinetics of growth of cervical cancer (CCM-1) transplanted on mice CBA, also the mitotic cycle and diurnal activity of tumor cells division. The tumor growth can well be described with the Hompertz equation, the constants of acceleration and retardation being equal to 0.34 day-1 and 0.004 day-1 accordingly. A linear dependence between the size, weight and number of CCM-1 celos is shown. In the tumor under study a persistant diurnal rhythm of the cell division was found with the maximum at 7 and 19 hours and the minimum at 13. The basis parameters of the mitotic cycle of tumor cells were determined: Tc=17.8 hr., G2 approximately 40 min.; S=9 hr., M approximately 24 min., G1 approximately 18.4 hr. The time of tumor doubling was 48.7 hr. The cell loss factor is as much as 42.1 per cent.
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J Cell Biol
March 2025
Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL) , Heidelberg, Germany.
How cells establish the interphase genome organization after mitosis is incompletely understood. Using quantitative and super-resolution microscopy, we show that the transition from a Condensin to a Cohesin-based genome organization occurs dynamically over 2 h. While a significant fraction of Condensins remains chromatin-bound until early G1, Cohesin-STAG1 and its boundary factor CTCF are rapidly imported into daughter nuclei in telophase, immediately bind chromosomes as individual complexes, and are sufficient to build the first interphase TAD structures.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Biochemistry, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
Renal cell carcinoma (RCC) is considered as a "metabolic disease" due to various perturbations in metabolic pathways that could drive cancer development. Glycine decarboxylase (GLDC) is a mitochondrial enzyme that takes part in the oxidation of glycine to support nucleotide biosynthesis via transfer of one-carbon units. Herein, we aimed to investigate the potential role of GLDC in RCC development.
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 PDFCell Death Dis
January 2025
Mater Research Institute, The University of Queensland, Brisbane, QLD, Australia.
Polyploidy is a common outcome of chemotherapies, but there is conflicting evidence as to whether polyploidy is an adverse, benign or even favourable outcome. We show Aurora B kinase inhibitors efficiently promote polyploidy in many cell types, resulting in the cell cycle exit in RB and p53 functional cells, but hyper-polyploidy in cells with loss of RB and p53 function. These hyper-polyploid cells (>8n DNA content) are viable but have lost long-term proliferative potential in vitro and fail to form tumours in vivo.
View Article and Find Full Text PDFPharmaceuticals (Basel)
December 2024
Laboratory of Molecular and Cellular Neurogenetics, N.N. Burdenko National Medical Research Center of Neurosurgery, 125047 Moscow, Russia.
Indolo[2,3-]pyrrolo[3,4-]carbazole scaffold is successfully used as an efficient structural motif for the design and development of different antitumor agents. In this study, we investigated the anti-glioblastoma therapeutic potential of glycosylated indolocarbazole analog LCS1269 utilizing in vitro, in vivo, and in silico approaches. Cell viability was estimated by an MTT assay.
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