To investigate the effects of ectodysplasin-A1 (EDA1) on the proliferation and cell cycle of ameloblast-like epithelial cells (LS8 cells). Wild EDA1 plasmid pCR3-Flag-EDA1-W (wild group), syndrome mutant EDA1 plasmid pCR3-Flag-EDA1-H252L (mutant group) and empty vector plasmid pCR3-Flag (control group) were transfected into LS8 cells. Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay and cell cycle was detected by flow cytometry. All tests were repeated three times. Compared with the control group (0.105±0.032), the proliferation activity of the wild group (0.201±0.009) was significantly higher after 72 h (<0.05). Compared with the control group (0.168±0.054) and the mutant group (0.194±0.059), the proliferation activity of the wild group (0.386±0.066) was significantly higher after 96 h (<0.05). There was no significant difference between the mutant group and the control group at all time points (>0.05). In the G/G phase, compared with the control group (65.4%±2.1%) and the mutant group (66.6%±3.1%), the cell distribution ratio of the wild group (51.2%±1.1%) was significantly lower (<0.01). In the S phase, compared with the control group (23.1%±2.0%) and the mutant group (21.9%±1.8%), the cell distribution ratio of the wild type group (37.3%±2.4%) was significantly higher (<0.01). There was no significant difference in cell cycle distribution between the mutant group and the control group (<0.05). Wild EDA1 promotes the proliferation of LS8 cells and the transformation from G/G to S phase. The syndrome mutant EDA1 (EDA1-H252L) loses its function of regulating the cell proliferation and cell cycle of LS8 cells.
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http://dx.doi.org/10.3760/cma.j.cn112144-20200816-00461 | DOI Listing |
J Neuroinflammation
January 2025
Department of Neuroscience and Experimental Therapeutics, School of Medicine, Texas A&M Health Science Center, Bryan, TX, 77807-3260, USA.
Background: Disturbances of the sleep-wake cycle and other circadian rhythms typically precede the age-related deficits in learning and memory, suggesting that these alterations in circadian timekeeping may contribute to the progressive cognitive decline during aging. The present study examined the role of immune cell activation and inflammation in the link between circadian rhythm dysregulation and cognitive impairment in aging.
Methods: C57Bl/6J mice were exposed to shifted light-dark (LD) cycles (12 h advance/5d) during early adulthood (from ≈ 4-6mo) or continuously to a "fixed" LD12:12 schedule.
Radiat Oncol
January 2025
Department of Radiation Oncology, Xijing Hospital, Air Force Medical University, Xi'an, 710032, Shaanxi, China.
Purpose: Based on the demonstration of a circadian rhythm in the human oral mucosa cell cycle, with most cells in the G2/M phase in the afternoon and at night, the present study evaluated the severity of acute radiation esophagitis and treatment outcomes in esophageal squamous cell carcinoma patients receiving radiotherapy (RT) in the daytime versus in the evening.
Methods: From the 488 eligible patients of esophageal squamous cell carcinoma receiving concurrent chemoradiotherapy (CCRT), 369 patients received RT in the daytime (before 19:00) and 119 patients received RT in the evening (after 19:00). The grades of radiation esophagitis (Common Terminology Criteria for Adverse Events version 5.
Exp Mol Med
January 2025
Department of Molecular Science and Technology, Ajou University, Suwon, South Korea.
Most cancer mutation profiling studies are laboratory-based and lack direct clinical application. For clinical use, it is necessary to focus on key genes and integrate them with relevant clinical variables. We aimed to evaluate the prognostic value of the dosage of the KRAS G12 mutation, a key pancreatic ductal adenocarcinoma (PDAC) variant and to investigate the biological mechanism of the prognosis associated with the dosage of the KRAS G12 mutation.
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 Differ
January 2025
Department of Immunology and Microbiology, University of Colorado, Anschutz Medical Campus, Aurora, CO, 80045, USA.
The assembly of Tcrb and Tcra genes require double negative (DN) thymocytes to undergo multiple rounds of programmed DNA double-strand breaks (DSBs), followed by their efficient repair. However, mechanisms governing cell cycle checkpoints and specific survival pathways during the repair process remain unclear. Here, we report high-resolution scRNA-seq analyses of individually sorted mouse DN3 and DN4 thymocytes, which reveals a G2M cell cycle checkpoint, in addition to the known G1 checkpoint, during Tcrb and Tcra recombination.
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