LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis
Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues bas...
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oai:doaj.org-article:1f87c665d88441e39d541ca8508568212021-12-01T14:41:00ZLncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis2165-59792165-598710.1080/21655979.2021.1994719https://doaj.org/article/1f87c665d88441e39d541ca8508568212021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1994719https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines. Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.DHRS4-AS1 expression was significantly correlated to tumor size (P = 0.02) and TNM stage (P = 0.045). CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. Our study provides lncRNA DHRS4-AS1/miR-522-3p/SOCS5 axis as a novel target for HCC therapeutic strategy with potentiality.Yongping ZhouKuan LiXuexia ZouZhiyuan HuaHao WangWuyang BianHong WangFangming ChenTu DaiTaylor & Francis Grouparticlehepatocellular carcinomadhrs4-as1mir-522-3psocs5proliferationBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 10862-10877 (2021) |
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hepatocellular carcinoma dhrs4-as1 mir-522-3p socs5 proliferation Biotechnology TP248.13-248.65 |
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hepatocellular carcinoma dhrs4-as1 mir-522-3p socs5 proliferation Biotechnology TP248.13-248.65 Yongping Zhou Kuan Li Xuexia Zou Zhiyuan Hua Hao Wang Wuyang Bian Hong Wang Fangming Chen Tu Dai LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
description |
Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines. Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.DHRS4-AS1 expression was significantly correlated to tumor size (P = 0.02) and TNM stage (P = 0.045). CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. Our study provides lncRNA DHRS4-AS1/miR-522-3p/SOCS5 axis as a novel target for HCC therapeutic strategy with potentiality. |
format |
article |
author |
Yongping Zhou Kuan Li Xuexia Zou Zhiyuan Hua Hao Wang Wuyang Bian Hong Wang Fangming Chen Tu Dai |
author_facet |
Yongping Zhou Kuan Li Xuexia Zou Zhiyuan Hua Hao Wang Wuyang Bian Hong Wang Fangming Chen Tu Dai |
author_sort |
Yongping Zhou |
title |
LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
title_short |
LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
title_full |
LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
title_fullStr |
LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
title_full_unstemmed |
LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis |
title_sort |
lncrna dhrs4-as1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via mir-522-3p/socs5 axis |
publisher |
Taylor & Francis Group |
publishDate |
2021 |
url |
https://doaj.org/article/1f87c665d88441e39d541ca850856821 |
work_keys_str_mv |
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