J Cancer 2020; 11(12):3604-3614. doi:10.7150/jca.41437
MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3
Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Nanjing, Jiangsu Province, China
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 http://www.jcancer.org/v11p3604.htm
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