The lncRNA B3GALT5-AS1 Functions as an HCC Suppressor by Regulating the miR-934/UFM1 Axis

Author:

Chen Erlin12,Zhou Bin3,Bian Saiyan45,Ni Wenkai46,Chen Zhong12ORCID

Affiliation:

1. Department of General Surgery, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, Jiangsu 215123, China

2. Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China

3. Departments of General Surgery, Suzhou Wuzhong People’s Hospital, Suzhou, Jiangsu 215100, China

4. Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China

5. Medical College, Nantong University, Nantong, Jiangsu 226001, China

6. Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China

Abstract

Accumulating evidence has demonstrated that long noncoding RNA (lncRNA) is importantly related to the occurrence and development of cancer. According to reports, the expression of B3GALT5-AS1 in hepatocellular carcinoma (HCC) is downregulated; however, the role of B3GALT5-AS1 in HCC is not yet clear. In this study, our purpose is to explore the biological function of B3GALT5-AS1 in HCC and its coupling mechanism with miR-934 and ubiquitin-fold modifier 1 (UFM1). We found that the B3GALT5-AS1 expression level was of significant reduction in both HCC tissues and cell lines; B3GALT5-AS1 overexpression (ov) may inhibit the malignant features of HCC. In addition, we demonstrated that miR-934 mimics could reverse the effect of B3GALT5-AS1 ov, which proved miR-934 was the downstream regulator of B3GALT5-AS1. Furthermore, si-UFM1 could reverse the effect of miR-934 inhibitor, which revealed the connection between them. Moreover, we found that B3GALT5-AS1 could keep down the PI3K/AKT pathway through UFM1. Our results demonstrated that B3GALT5-AS1 was an excellent HCC suppressant by regulating miR-934 and UFM1 to achieve negative regulation of HCC cell proliferation, invasion, and metastasis, indicating that B3GALT5-AS1 is a promising potential therapeutic target for HCC treatment.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Oncology

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