期刊
ONCOTARGET
卷 7, 期 4, 页码 4735-4745出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6732
关键词
autophagy; UVRAG; miR-183; apoptosis; colorectal cancer
资金
- National Basic Research Program of China (973 program) [2013CB531104]
- Funds for Creative Research Groups of the National Natural Science Foundation of China [81421063]
- National Natural Science Foundation of China [81230081, 31450009]
- Postgraduate Research Innovation Fund of Harbin Medical University [YJSCX2014-13HYD]
Ultraviolet radiation resistance-associated gene (UVRAG) is a well-known regulator of autophagy by promoting autophagosome formation and maturation. Multiple studies have implicated UVRAG in the pathogenesis of colorectal cancer. However, the mechanisms underlying the regulation of UVRAG are unclear. Here, we describe miR-183 as a new autophagy-inhibiting miRNA. Our results showed that induction of autophagy lead to down-regulation of miR-183 in colorectal cancer cells. And, over-expression of miR-183 resulted in the attenuation of rapamycinor starvation-induced autophagy in cancer cells, whereas inhibition of endogenous miR-183 stimulated autophagy and apoptosis. Additionally, either autophagy inhibitor 3-MA or pan-caspase inhibitor Z-VAD-FMK respectively or both treatments reversed AMO-183-induced cell death. Further studies showed that UVRAG is a target of miR183 and as a key regulator promotes autophagy and apoptosis. More importantly, overexpression of UVRAG rescued autophagic activity and induced apoptosis in presence of miR-183. Therefore, the present study investigated the promoting effect of miR-183 on colorectal cancer progression, which was considered to be mediated by autophagy and apoptosis through targeting of UVRAG.
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