Journal
CANCER LETTERS
Volume 362, Issue 2, Pages 183-191Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2015.03.045
Keywords
Mitochondrial fission; Cisplatin sensitivity; miR-483-5p; FIS1; Tongue squamous cell carcinoma
Categories
Funding
- National Natural Science Foundation of China [81472521, 81272951, 81072225, 81172563, 81402251, 81302369]
- Natural Science Foundation of Guangdong Province [10251008901000022]
- Fund for Excellent Doctoral Dissertation of Guangdong Province [81000-3212502]
- Fundamental Research Funds for the Central Universities [13ykpy27]
- Specialized Research Fund for the Doctoral Program of Higher Education [20110171110068]
- Science and Technology Project of Guangzhou City [2012J4100078]
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Mitochondria play an important role in the initiation of apoptosis. However, whether cisplatin can induce apoptosis by initiating a mitochondrial fission pathway and the mechanism underlying this effect remain poorly understood. In this study, we show that the mitochondrial fission protein FIS1 is upregulated upon cisplatin treatment in tongue squamous cell carcinoma (TSCC) cells. FIS1 knockdown can attenuate mitochondrial fission and cisplatin sensitivity. We found that FIS1 is a direct target of miR-483-5p and that miR-483-5p can inhibit mitochondrial fission and cisplatin sensitivity in vitro and in vivo. Furthermore, we found that miR-483-5p and FIS1 are significantly associated with cisplatin sensitivity and with overall survival in patients with TSCC in a retrospective analysis of multiple centers. This study revealed that a novel mitochondrial fission pathway composed of miR-483-5p and FIS1 regulates cisplatin sensitivity. The modulation of miR-483-5p and FIS1 levels may provide a new approach for increasing cisplatin sensitivity. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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