Редактирование: TRIB2 (раздел)

==Publications==

{{medline-entry
|title=[[TRIB2]] functions as novel oncogene in colorectal cancer by blocking cellular senescence through AP4/p21 signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30541550
|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.
|mesh-terms=* Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
* Calcium-Calmodulin-Dependent Protein Kinases
* Cell Cycle
* Cell Cycle Checkpoints
* Cell Line
* Cell Proliferation
* Cellular Senescence
* Colorectal Neoplasms
* Cyclin-Dependent Kinase Inhibitor p21
* DNA-Binding Proteins
* HEK293 Cells
* Humans
* Intracellular Signaling Peptides and Proteins
* Oncogenes
* RNA-Binding Proteins
* Signal Transduction
|keywords=* AP4
* Cellular senescence
* Colorectal cancer
* TRIB2
* p21
* p53
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291992
}}