期刊
CANCER RESEARCH
卷 71, 期 13, 页码 4628-4639出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-10-2475
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资金
- National Institute of Biomedical Innovation (NIBIO)
- Ministry of Health, Labor and Welfare, Japan
- Takeda Science Foundation
- Ministry of Education, Culture, Sports & Technology of Japan
- Foundation for Promotion of Cancer Research Japan
- Grants-in-Aid for Scientific Research [20221009, 23300359] Funding Source: KAKEN
Selective activation of p53 target genes in response to various cellular stresses is a critical step in determining the ability to induce cell-cycle arrest or apoptosis. Here we report the identification of the microRNA miR-22 as a p53 target gene that selectively determines the induction of p53-dependent apoptosis by repressing p21. Combinatorial analyses of the AGO2 immunocomplex and gene expression profiles identified p21 as a direct target of miR-22. Induction of p21 was inhibited by miR-22 after exposure to the genotoxic agent Adriamycin (doxorubicin; Bedford Laboratories), sensitizing cells to p53-dependent apoptosis. Interestingly, the activation of miR-22 depended on the intensity of the stresses that induced cells to undergo apoptosis in the presence of p21 suppression. Our findings define an intrinsic molecular switch that determines p53-dependent cellular fate through post-transcriptional regulation of p21. Cancer Res; 71(13); 4628-39. (C)2011 AACR.
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