J Cancer 2020; 11(12):3604-3614. doi:10.7150/jca.41437 This issue

Research Paper

MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3

Jia Wei Zhang*, Xing Wang*, Gao Chao Li, Dong Wang, Sheng Han, Yao Dong Zhang, Chen Huan Luo, Hong Wei Wang, Wang Jie Jiang, Chang Xian Li, Xiang Cheng Li

Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Nanjing, Jiangsu Province, China
*Equal contributors

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Zhang JW, Wang X, Li GC, Wang D, Han S, Zhang YD, Luo CH, Wang HW, Jiang WJ, Li CX, Li XC. MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3. J Cancer 2020; 11(12):3604-3614. doi:10.7150/jca.41437. Available from https://www.jcancer.org/v11p3604.htm

File import instruction


Background: MicroRNAs (miRNAs) play important roles in the occurrence and development of cancers. In this project, we aimed to explore the role and molecular mechanism of mir-30a-5p in cholangiocarcinoma (CCA).

Materials and Methods: The expression profile and clinical significance of miR-30a-5p in CCA patients were investigated in 31 ICC and 52 ECC patients respectively. The role and mechanism of miR-30a-5p in CCA cells were investigated by up-regulating and inhibiting miR-30a-5p expression in vitro functional study.

Results: The expression of miR-30a-5p was increased in both CCA tissues and cells. The inhibition of miR-30a-5p decreased cell proliferation and induced cell apoptosis while overexpression of miR-30a-5p achieved the opposite effect. Furthermore, SOCS3 was down-regulated in ICC and ECC tissues and negatively regulated by miR-30a-5p. Dual-luciferase reporter assay revealed that co-transfection of miR-30a-5p significantly inhibited the activity of firefly luciferase reporter carrying the wild-type 3′UTR of SOCS3. The inhibition of SOCS3 could largely rescue the inhibitory effect of miR-30a-5p inhibition on CCA cells proliferation. In clinical, up-regulated miR-30a-5p expression was correlated with large tumor size in both ICC and ECC cohorts.

Conclusions: miR-30a-5p promoted CCA cells proliferation through targeting SOCS3. These findings suggested that miR-30a-5p could be a potential therapeutic target.

Keywords: miR-30a-5p, cholangiocarcinoma, SOCS3, proliferation, apoptosis