Research Papers:

MicroRNA-212 suppresses tumor growth of human hepatocellular carcinoma by targeting FOXA1

Changwei Dou, Yufeng Wang, Chao Li, Zhikui Liu, Yuli Jia, Qing Li, Wei Yang, Yingmin Yao, Qingguang Liu and Kangsheng Tu _

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Oncotarget. 2015; 6:13216-13228. https://doi.org/10.18632/oncotarget.3916

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Changwei Dou1, Yufeng Wang1, Chao Li1, Zhikui Liu1, Yuli Jia1, Qing Li1, Wei Yang1, Yingmin Yao1, Qingguang Liu1 and Kangsheng Tu1

1 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China

Correspondence to:

Kangsheng Tu, email:

Qingguang Liu, email:

Keywords: MiR-212, FOXA1, hepatocellular carcinoma, proliferation, apoptosis

Received: February 02, 2015 Accepted: March 31, 2015 Published: April 23, 2015


MicroRNA-212 (miR-212) has been reported to play oncogenic or tumor suppressive role in different human malignancies. Here, we demonstrated that the mean level of miR-212 in hepatocellular carcinoma (HCC) tissues was significantly lower than that in matched tumor-adjacent tissues. Similarly, the expression of miR-212 was obviously reduced in HCC cell lines as compared with a nontransformed hepatic cell line. Ectopic expression of miR-212 inhibited cell viability and proliferation, and induced apoptosis in HepG2 cells. In contrast, down-regulation of miR-212 increased cell viability and proliferation, and suppressed apoptosis in Bel-7402 cells. In vivo studies showed that miR-212 inhibited tumor growth of HCC via suppressing proliferation and inducing apoptosis. Furthermore, we confirmed that Forkhead box protein A1 (FOXA1) was a direct target of miR-212, and it abrogated the function of miR-212 in HCC. Finally, we disclosed that the aberrant expression of miR-212 and FOXA1 was evidently correlated with poor prognostic features of HCC. MiR-212, FOXA1 and their combination were valuable prognostic markers for predicting survival of HCC patients. In conclusion, miR-212 may serve as a prognostic indicator for HCC patients and exerts tumor suppressive role, at least in part, by inhibiting FOXA1.

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