Int J Biol Sci 2021; 17(2):623-634. doi:10.7150/ijbs.55020 This issue

Research Paper

MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis

Weiwei Chen1*, Kundong Zhang1*, Yuhan Yang1, Zengya Guo1, Xiaofeng Wang1, Buwei Teng2, Qian Zhao3✉, Chen Huang1✉, Zhengjun Qiu1✉

1. Department of General Surgery, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, 100 Haining Road, Shanghai, 201600, China.
2. Lianyungang Clinical College of Nanjing Medical University/The First People's Hospital of Lianyungang, 6 Zhenhua East Road, Haizhou District, City of Lianyungang, Jiangsu Province, 222061, China.
3. Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
* These authors contributed equally to this work.

This is an open access article distributed under the terms of the Creative Commons Attribution License ( See for full terms and conditions.
Chen W, Zhang K, Yang Y, Guo Z, Wang X, Teng B, Zhao Q, Huang C, Qiu Z. MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis. Int J Biol Sci 2021; 17(2):623-634. doi:10.7150/ijbs.55020. Available from

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Graphic abstract

Background: Long non-coding RNAs (lncRNAs) are deemed to be relevant to the tumorigenesis and development of a variety of tumors, containing gastric cancer (GC). The purpose of our investigations is to explore the character of HCP5 in GC.

Methods: HCP5 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in 62 matched GC tissues and corresponding para-carcinoma tissues. In vitro and in vivo functional assays were subjected to verify the biological effects of HCP5 after alteration of HCP5. Chromatin immunoprecipitation assay (CHIP) assays were conducted to confirm that myocyte enhancer factor 2A (MEF2A) could bind to HCP5 promoter regions and thereby induce HCP5 expression. Analysis of the latent binding of miR-106b-5p to HCP5 and p21 was made by bioinformatics prediction and luciferase reporter assays.

Results: Significant downregulation of HCP5 was detected in GC tissues. Negative correlation was determined between HCP5 expression level and tumor size and overall survival in GC patients. HCP5 depletion had a facilitating impact on proliferation, migration and invasion of GC cells. Consistently, overexpression of HCP5 came into an opposite effect. Moreover, we demonstrated that MEF2A could combine with the promoter region of HCP5 and thereby induce HCP5 transcription. Luciferase reporter assays revealed that HCP5 could compete with miR-106b-5p as a competing endogenous RNA (ceRNA) and upregulated p21 expression in GC.

Conclusions: MEF2A-mediated HCP5 could exert an anti-tumor effect among the development of GC via miR-106b-5p/p21 axis, which provides a novel target for GC therapy.

Keywords: HCP5, MEF2A, Competing endogenous RNA, miR-106b-5p/p21 axis, Gastric Cancer.