Research Paper Volume 14, Issue 4 pp 1767—1781
The novel lncRNA GPC5-AS1 stabilizes GPC5 mRNA by competitively binding with miR-93/106a to suppress gastric cancer cell proliferation
- 1 Department of Cell Biology and Genetics, Key Laboratory of Environment and Genes Related to Diseases, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, P.R. China
- 2 Institute of Genetics and Developmental Biology, Translational Medicine Institute, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center, Xi’an, P.R. China
- 3 Department of Gastroenterology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China
- 4 Key Laboratory of Environment and Genes Related to Diseases, Xi’an Jiaotong University, Ministry of Education of China, Xi’an, P.R. China
- 5 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China
- 6 Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Xi’an, P.R. China
Received: October 30, 2021 Accepted: February 8, 2022 Published: February 18, 2022
https://doi.org/10.18632/aging.203901How to Cite
Copyright: © 2022 Bo 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
Long non-coding RNAs (lncRNAs) are of importance in the genesis and progression of gastric cancer (GC). GPC5-AS1 is a novel lncRNA associated with methyl-CpG-binding protein 2 (MeCP2), identified in our previous microarray analysis; however, the role of GPC5-AS1 in GC remains unknown. In the present study, we demonstrate that GPC5-AS1 is downregulated in GC cells and tissues, and this aberrant expression is regulated by MeCP2 through CpG site binding in the promoter region. Importantly, we also demonstrate that GPC5-AS1 overexpression suppresses cell proliferation, colony formation, and cell cycle transition; induces apoptosis in vitro; and inhibits tumorigenicity in vivo. The expression of the controversial gene GPC5 was downregulated in GC tissues, and elevated GPC5 level could inhibit GC cell growth. Mechanistically, we demonstrated that GPC5-AS1 stabilizes GPC5 mRNA by acting as a molecular sponge for miR-93 and miR-106a, thereby reducing GC tumor progression. In conclusion, our results suggest that GPC5-AS1 may play a pivotal role in GC and serve as a potential diagnostic biomarker and a powerful therapeutic target for GC.