https://transhumanist.ru/index.php?action=history&feed=atom&title=TRIB2 2026-05-01T18:17:28Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=TRIB2&diff=4434&oldid=prev 2021-04-29T19:17:56Z

<p>Новая страница: «Tribbles homolog 2 (TRB-2) [TRB2] ==Publications== {{medline-entry |title=<a href="/TRIB2" title="TRIB2">TRIB2</a> functions as novel oncogene in colorectal cancer by blocking cellular senesc...»</p> <p><b>Новая страница</b></p><div>Tribbles homolog 2 (TRB-2) [TRB2]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=[[TRIB2]] functions as novel oncogene in colorectal cancer by blocking cellular senescence through AP4/p21 signaling.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30541550<br /> |abstract=Cellular senescence is a state of irreversible cell growth arrest and senescence cells permanently lose proliferation potential. Induction of cellular senescence might be a novel therapy for cancer cells. [[TRIB2]] has been reported to participate in regulating proliferation and drug resistance of various cancer cells. However, the role of [[TRIB2]] in cellular senescence of colorectal cancer (CRC) and its molecular mechanism remains unclear. The expression of [[TRIB2]] in colorectal cancer tissues and adjacent tissues was detected by immunohistochemistry and RT-PCR. The growth, cell cycle distribution and cellular senescence of colorectal cancer cells were evaluated by Cell Counting Kit-8 (CCK8) assay, flow cytometry detection and senescence-associated β-galactosidase staining, respectively. Western blot, RT-PCR and luciferase assay were performed to determine how [[TRIB2]] regulates p21. Immunoprecipitation (IP) and chromatin-immunoprecipitation (ChIP) were used to investigate the molecular mechanisms. We found that [[TRIB2]] expression was elevated in CRC tissues compared to normal adjacent tissues and high [[TRIB2]] expression indicated poor prognosis of CRC patients. Functionally, depletion of [[TRIB2]] inhibited cancer cells proliferation, induced cell cycle arrest and promoted cellular senescence, whereas overexpression of [[TRIB2]] accelerated cell growth, cell cycle progression and blocked cellular senescence. Further studies showed that [[TRIB2]] physically interacted with AP4 and inhibited p21 expression through enhancing transcription activities of AP4. The rescue experiments indicated that silencing of AP4 abrogated the inhibition of cellular senescence induced by [[TRIB2]] overexpression. These data demonstrate that [[TRIB2]] suppresses cellular senescence through interaction with AP4 to down-regulate p21 expression. Therefore, [[TRIB2]] could be a potential target for CRC treatment.<br /> |mesh-terms=* Basic Helix-Loop-Helix Leucine Zipper Transcription Factors<br /> * Calcium-Calmodulin-Dependent Protein Kinases<br /> * Cell Cycle<br /> * Cell Cycle Checkpoints<br /> * Cell Line<br /> * Cell Proliferation<br /> * Cellular Senescence<br /> * Colorectal Neoplasms<br /> * Cyclin-Dependent Kinase Inhibitor p21<br /> * DNA-Binding Proteins<br /> * HEK293 Cells<br /> * Humans<br /> * Intracellular Signaling Peptides and Proteins<br /> * Oncogenes<br /> * RNA-Binding Proteins<br /> * Signal Transduction<br /> |keywords=* AP4<br /> * Cellular senescence<br /> * Colorectal cancer<br /> * TRIB2<br /> * p21<br /> * p53<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291992<br /> }}</div>

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