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Research Paper|Volume 13, Issue 12|pp 16267—16286

Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A

Yongping Zhou1, Kuan Li4, Tu Dai1, Hong Wang1, Zhiyuan Hua1, Wuyang Bian1, Hao Wang1, Fangming Chen3, Xiaoming Ai2
  • 1Department of Hepatobiliary Surgery, Wuxi Second Hospital, Nanjing Medical University, Wuxi, Jiangsu, China
  • 2Department of General Surgery, BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
  • 3Department of Imaging, Wuxi Second Hospital, Nanjing Medical University, Wuxi, Jiangsu, China
  • 4Department of Hepatobiliary Surgery, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, Jiangsu, China
* Equal contribution
Received: September 30, 2020Accepted: January 21, 2021Published: June 18, 2021
https://doi.org/10.18632/aging.203155

Copyright: © 2021 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Multiple studies have revealed that long non-coding RNA (lncRNAs) served as regulatory factors in modulating tumorigenesis of hepatocellular carcinoma (HCC). In the present study, we demonstrated that lncRNA HCP5 was overexpressed in HCC tissues and cell lines, and these findings were obvious even in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis, and invasion both in vitro and in vivo through promoting apoptosis and by inactivating the epithelial-mesenchymal transition (EMT) progress. Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, and served as a tumor suppressor of HCC to prevent cell proliferation, migration, and invasion. Subsequently, DNMT3A was identified as a downstream regulatory factor of miR-29b-3p, and acted as a participated element of HCC progression by activating AKT phosphorylation. Taken together, our study elucidated for the first time that HCP5 plays a crucial role in HCC via the HCP5/miR-29b-3p/DNMT3A/AKT axis and our findings demonstrated a novel diagnostic and therapeutic strategy with potentiality to treat HCC.