Cancer Management and Research (Nov 2021)
LncRNA DNAJC3-AS1 Promotes Hepatocellular Carcinoma (HCC) Progression via Sponging Premature miR-27b
Abstract
Changbo Fu,1 Jianxiu Li,2 Ping Li,3 Dan Cheng4 1Department of Hepatobiliary and Pancreatic Surgery, Hubei Cancer Hospital, Wuhan City, 430000, People’s Republic of China; 2Disinfection Supply Center of Weifang Yidu Central Hospital, Weifang City, 266000, People’s Republic of China; 3Emergency Care Center of Qingdao Central Hospital, Qingdao City, 266000, People’s Republic of China; 4Department of Liver Disease Infection, Edong Healthcare City Hospital of Traditional Chinese Medicine, Infections Disease Hospital, Huangshi City, 435000, People’s Republic of ChinaCorrespondence: Dan ChengDepartment of Liver Disease Infection, Edong Healthcare City Hospital of Traditional Chinese Medicine, Infections Disease Hospital, No. 634 Shenxia Road, Huangshi City, 435000, People’s Republic of ChinaEmail [email protected]: Long non-coding RNA (lncRNA) DNAJC3 antisense RNA 1 (head to head) (DNAJC3-AS1) plays a key role in the progression of several cancers. However, its biological role in hepatocellular carcinoma (HCC) is still unclear. We aimed to investigate the role of DNAJC3-AS1 in the development of HCC and reveal the potential mechanisms.Materials and Methods: Expression analysis of DNAJC3-AS1 and microRNA-27b (miR-27b) at both mature and premature levels was determined by RT-qPCR. HCC patients were followed up for 5 years to analyze the prognostic value of DNAJC3-AS1 for HCC. The direct interaction between DNAJC3-AS1 and premature miR-27b was analyzed with RNA pull-down assay. Subcellular analysis of DNAJC3-AS1 was explored by subcellular fractionation assay. DNAJC3-AS1 overexpression and knockdown were carried out to analyze the role of DNAJC3-AS1 in miR-27b maturation. Cell proliferation was analyzed by BrdU assay.Results: DNAJC3-AS1 was overexpressed in HCC and predicts the poor survival. MiR-27b was downregulated at mature miRNA level, but upregulated at premature level. DNAJC3-AS1 directly interacted with premature miR-27b and was localized to both nuclear and cytoplasm. DNAJC3-AS1 overexpression upregulated premature miR-27b and downregulated mature miR-27b, while DNAJC3-AS1 knockdown led to the opposite results. DNAJC3-AS1 suppressed the role of miR-27b in inhibiting cell proliferation.Conclusion: DNAJC3-AS1 promotes HCC by sponging premature miR-27b and might be a biomarker and therapeutic target for HCC.Keywords: DNAJC3-AS1, miR-27b, hepatocellular carcinoma, maturation
