期刊
AUTOPHAGY
卷 16, 期 7, 页码 1186-1199出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2019.1659614
关键词
Autophagy; long noncoding RNA; MTOR; tumorigenesis; uveal melanoma
类别
资金
- National Key Research and Development Plan [2017YFE0196300]
- National Natural Science Foundation of China [81772875, 31470757, 91754205, 31771523, 31870748]
- ShuGuang Project of Shanghai Municipal Education Commission [17SG19]
- Shanghai Education Development Foundation [17SG19]
- Program for Professor of Special Appointment (Eastern Scholar) at the Shanghai Institutions of Higher Learning [1410000159]
- Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant [20161317]
- Science and Technology Commission of Shanghai [16ZR1419600, 17DZ2260100]
- Outstanding Yong Medical Scholar of Shanghai Municipal Commission of Health and Family Planning [2017YQ067]
Long noncoding RNAs (lncRNAs) are proved to be critical regulators in numerous cellular processes. However, the potential involvement of lncRNAs in macroautophagy/autophagy is largely unknown. Autophagy is a highly regulated cellular degradation system, and its dysregulation is involved in many human diseases, including cancers. Here, we show that the lncRNA ZNNT1 is induced by PP242 and MTORC1 selective inhibitor rapamycin in uveal melanoma (UM) cells. Overexpression of ZNNT1 promotes autophagy by upregulating ATG12 expression, whereas knockdown of ZNNT1 attenuates PP242-induced autophagy. Overexpression of ZNNT1 inhibits tumorigenesis and the migration of UM cells, and knockdown of ATG12 can partially rescue the ZNNT1-induced inhibition of UM tumorigenesis. In summary, our study reveals that ZNNT1 acts as a potential tumor suppressor in UM by inducing autophagy.
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