miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway

  • iScience. 2021 Oct 14;24(11):103271. doi: 10.1016/j.isci.2021.103271.
Sijie Xie  1 ,  Xiaoxue Jiang  1 ,  Rushi Qin  1 ,  Shuting Song  1 ,  Yanan Lu  1 ,  Liyan Wang  1 ,  Yingjie Chen  1 ,  Dongdong Lu  1
Affiliations
  • 1. Shanghai Putuo People's Hospital, School of Life Science and Technology, Tongji University, 200092 Shanghai, China.
PMID: 34761190 DOI: 10.1016/j.isci.2021.103271
Abstract

miR-1307 is highly expressed in liver Cancer and inhibits methyltransferase protein8. Thereby, miR-1307 inhibits the expression of KDM3A and KDM3B and increases the methylation modification of histone H3 lysine 9, which enhances the expression of endoplasmic-reticulum-related gene CALR. Of note, miR-1307 weakens the binding ability of OSTC to CDK2, CDK4, CyclinD1, and cyclinE and enhances the binding ability of CALR to CDK2, CDK4, CyclinD1, and cyclinE, decreasing of p21WAF1/CIP1, GADD45, pRB, and p18, and decreasing of ppRB. Furthermore, miR-1307 increases the activity of H-Ras, PKM2, and PLK1. Strikingly, miR-1307 reduces the binding ability of OSTC to Atg4 and enhances the binding ability of CALR to Atg4. Therefore, miR-1307 reduces the occurrence of Autophagy based on ATG4-LC3-ATG3-ATG7-ATG5-ATG16L1-ATG12-ATG9- Beclin1. In particular, miR-1307 enhances the expression of PAK2, PLK1, PRKAR2A, MYBL1, and Trim44 and inhibits the expression of Sash1 and SMAD5 via Autophagy. Our observations suggest that miR-1307 promotes hepatocarcinogenesis by CALR-OSTC-endoplasmic reticulum protein folding pathway.

Keywords
Cancer; Cell biology; Molecular biology.
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