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| Long noncoding RNA HAND2-AS1 re duce d the viability of hepatocellular carcinoma via targeting microRNA-300/SOCS5 axis |
| Hua-Qiang Bi a , # , Zhong-Hui Li b , # , Hui Zhang c , ∗ |
a Department of Hepatobiliary Surgery, First Affiliated Hospital of Third Military Medical University (Army Medical University), Chongqing 400038, China
b Department of Radiology, First Affiliated Hospital of Third Military Medical University (Army Medical University), Chongqing 400038, China
c Department of Vascular Surgery, First Affiliated Hospital of Third Military Medical University (Army Medical University), Chongqing 400038, China
∗ Corresponding author.
E-mail address: huizhangshj@163.com (H. Zhang).
# Contributed equally. |
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Abstract Background: Hepatocellular carcinoma (HCC) is one of the most prevalent human cancers with high mortality. Long non-coding RNA heart and neural crest derivatives expressed 2 anti-sense 1 (HAND2-AS1) is down-regulated in several cancers including HCC, yet the precise mechanisms how HAND2-AS1 regulates cell survival in HCC remains poorly understood.
Methods: The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR. The protein levels of suppressor of cytokine signaling 5 (SOCS5), Bcl-2, Bax and cleaved caspase-3 were determined by Western blot. Cell viability and cell proliferation were assessed using cell counting kit-8 and clone formation assay, respectively. Cell apoptosis was detected using flow cytometry. The interactions between HAND2-AS1 and miR-300, miR-300 and SOCS5 were validated using luciferase reporter assay.
Results: HAND2-AS1 was down-regulated in HCC tissues and cell lines, and the expression level of HAND2-AS1 was positively correlated to patient survival. HAND2-AS1 over-expression reduced viability and proliferation in HCC cells. Elevated HAND2-AS1 level induced apoptosis in HCC cells, accompanied with increased Bax and cleaved caspase-3 levels and decreased Bcl-2 level. We also validated that HAND2-AS1 acted as a sponge of miR-300, and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues. Furthermore, we found that SOCS5 was a downstream target of miR-300. In addition, miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation. miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.
Conclusion: lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS5 axis.
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2020, Vol. 19 
