期刊
BIOLOGICAL & PHARMACEUTICAL BULLETIN
卷 38, 期 4, 页码 618-624出版社
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b15-00003
关键词
Tribbles 1 (TRB1); p53; histone deacetylase 1 (HDAC1); deacetylation
资金
- Japan Society for the Promotion of Science (JSPS) [24590085]
- JSPS [24700983]
- Research Foundation for Pharmaceutical Sciences
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Takeda Science Foundation
- Suzuken Memorial Foundation
- Nakatomi Foundation
- Hori Sciences & Arts Foundation
- YOKOYAMA Foundation for Clinical Pharmacology [YRY1408]
- Grants-in-Aid for Scientific Research [15K07937, 15K07936, 24590085, 24700983] Funding Source: KAKEN
Tribbles 1 (TRB1) is one of the mammalian orthologs of Drosophila Tribbles, which regulates development and cell proliferation. TRB1 is suggested to act as a scaffold protein in signaling pathways for important cellular processes. TRB1 has also been identified as a myeloid oncogenic driver and mediates leuke-mogenesis through the mitogen-activated protein extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway and CCAAT/enhancer binding protein (C/EBP) transcriptional factors. However, the physiological roles of TRB1 in solid tumors have not been clarified. Here, we show that TRB1 interacts with p53 and suppresses its tumor suppressor activity. TRB1 knockdown enhances transcriptional activity of p53 and decreases cell viability. Interestingly, TRB1 enhances histone deacety lase 1 (HDAC1)-mediated p53 deacetylation and decreases DNA binding of p53. These results suggest that TRB1 is involved in the proliferation of tumor cells by inhibiting the activities of tumor suppressor p53 in solid tumors.
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