长链非编码RNA DNAJC3-AS1通过海绵化早熟的miR-27b促进肝细胞癌（HCC）进展。
LncRNA DNAJC3-AS1 Promotes Hepatocellular Carcinoma (HCC) Progression via Sponging Premature miR-27b.
作者信息
Fu Changbo, Li Jianxiu, Li Ping, Cheng Dan
机构信息
Department of Hepatobiliary and Pancreatic Surgery, Hubei Cancer Hospital, Wuhan City, 430000, People's Republic of China.
Disinfection Supply Center of Weifang Yidu Central Hospital, Weifang City, 266000, People's Republic of China.
出版信息
Cancer Manag Res. 2021 Nov 15;13:8575-8583. doi: 10.2147/CMAR.S321111. eCollection 2021.
PURPOSE
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.
目的
长链非编码RNA（lncRNA）DNAJC3反义RNA 1（头对头）（DNAJC3-AS1）在多种癌症进展中起关键作用。然而，其在肝细胞癌（HCC）中的生物学作用仍不清楚。我们旨在研究DNAJC3-AS1在HCC发生发展中的作用并揭示潜在机制。
材料与方法
通过RT-qPCR测定DNAJC3-AS1和微小RNA-27b（miR-27b）在成熟和前体水平的表达分析。对HCC患者进行5年随访以分析DNAJC3-AS1对HCC的预后价值。用RNA下拉实验分析DNAJC3-AS1与前体miR-27b之间的直接相互作用。通过亚细胞分级分离实验探索DNAJC3-AS1的亚细胞定位。进行DNAJC3-AS1过表达和敲低实验以分析DNAJC3-AS1在miR-27b成熟中的作用。通过BrdU实验分析细胞增殖。
结果
DNAJC3-AS1在HCC中过表达并预示不良生存。miR-27b在成熟miRNA水平下调，但在前体水平上调。DNAJC3-AS1与前体miR-27b直接相互作用，且定位于细胞核和细胞质。DNAJC3-AS1过表达上调前体miR-27b并下调成熟miR-27b，而DNAJC3-AS1敲低导致相反结果。DNAJC3-AS1抑制miR-27b在抑制细胞增殖中的作用。
结论
DNAJC3-AS1通过吸附前体miR-27b促进HCC，可能是HCC的生物标志物和治疗靶点。
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