Journal
ONCOGENE
Volume 35, Issue 24, Pages 3139-3150Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.370
Keywords
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Funding
- National Basic Research Program of China [2012CBA01302]
- National Natural Science Foundation of China [81425016, 81270646, 31171398]
- Natural Science Foundation of Guangdong Province [S2013030013305, 2015A030312013]
- Key Scientific and Technological Projects of Guangdong Province [2014B020226002, 2015B020226004, 2014B020228003, 2007A032100003]
- Key Scientific and Technological Program of Guangzhou City [201400000003-3, 201508020262, 201300000089, 2010U1-E00551]
- Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (GDUPS)
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Nestin is widely expressed in numerous tumors and has become a diagnostic and prognostic indicator. However, the exact mechanism by which nestin contributes to tumor malignancy remains poorly understood. Here, we found marked upregulation of nestin expression in highly proliferative and invasive gastrointestinal stromal tumor (GIST) specimens. Nestin knockdown in GIST cells reduced the proliferative and invasive activity owing to a decrease of mitochondrial intracellular reactive oxygen species (ROS) generation. Furthermore, nestin was co-localized with mitochondria, and knockdown of nestin increased mitochondrial elongation and influenced the mitochondrial function, including oxygen consumption rates, ATP generation and mitochondrial membrane potential and so on. In exploring the underlying mechanism, we demonstrated nestin knockdown inhibited the mitochondrial recruitment of Dynamin-related protein1 and induced the change of mitochondrial dynamics. Thus, nestin may have an important role in GIST malignancy by regulating mitochondrial dynamics and altering intracellular ROS levels. The findings provide new clues to reveal mechanisms by which nestin mediates the proliferation and invasion of GISTs.
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