Featured Discovery

Home > Featured Discovery > SJTU Research Teams Jointly Found New Mechanism of UM Autophagy

SJTU Research Teams Jointly Found New Mechanism of UM Autophagy

September 23, 2019      Author:

On September 3rd, Prof. Fan Xianqun's research team from Shanghai Ninth People's Hospital and Prof. Zhong Qing's research team from the College of Basic Medical Sciences jointly published the paper ZNNT1 Long Noncoding RNA Induces Autophagy to Inhibit Tumorigenesis of Uveal Melanoma by Regulating Key Autophagy Gene Expression on the Autophagy (IF=11.059). The paper demonstrates lncRNA ZNNT1 suppresses the tumorigenesis and the migration of Uveal Melanoma by regulating the key gene ATG12 and inducing autophagy in tumor cells.

Postgraduates Li Peng, He Jie, and Yang Zhi are the first authors of the paper; Fan Xianqun, Zhong Qing, and Zhang He are the corresponding authors; and Prof. Ge Shengfang also contributed to the paper. The paper was also funded by the National Key R&D Program of China, National Natural Science Foundation of China, and Science and Technology Commission Shanghai Municipality.


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.


Translated by Huang Yiqing  Reviewed by Wang Bingyu