Journal
CANCER RESEARCH
Volume 75, Issue 18, Pages 3890-3901Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-15-0257
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Funding
- Japan Society for the Promotion of Science (JSPS) [25250019, 24590372, 22134002]
- Japan Agency for Medical Research and Development
- Global Center of Excellence (GCOE) Program from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan
- Foundation for Promotion of Cancer Research from the Ministry of Health, Labour and Welfare (MHLW), Japan [H24-the 3rd Term-Young-002]
- Grants-in-Aid for Scientific Research [26670815, 24590372, 25250019, 15K08301, 15H05908, 26293067] Funding Source: KAKEN
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Some tumor-suppressing miRNAs target multiple oncogenes concurrently and therefore may be useful as cancer therapeutic agents. Further, such miRNAs may be useful to address chemotherapeutic resistance in cancer, which remains a primary clinical challenge in need of solutions. Thus, cytoprotective processes upregulated in cancer cells that are resistant to chemotherapy are a logical target for investigation. Here, we report that overexpression of miR-634 activates the mitochondrial apoptotic pathway by direct concurrent targeting of genes associated with mitochondrial homeostasis, antiapoptosis, antioxidant ability, and autophagy. In particular, we show how enforced expression of miR-634 enhanced chemotherapyinduced cytotoxicity in a model of esophageal squamous cell carcinoma, where resistance to chemotherapy remains clinically problematic. Our findings illustrate how reversing miR-634-mediated cytoprotective processes may offer a broadly useful approach to improving cancer therapy. (C) 2015 AACR.
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