Published online May 28, 2021. doi: 10.3748/wjg.v27.i20.2586
Peer-review started: November 18, 2020
First decision: January 23, 2021
Revised: February 10, 2021
Accepted: April 2, 2021
Article in press: April 2, 2021
Published online: May 28, 2021
Hepatocellular carcinoma (HCC) is a malignancy found globally.
The function of long noncoding RNAs (lncRNAs) in HCC requires further investigation.
We aimed to understand the effect of lncRNA W42 on HCC and dissect the underlying molecular mechanisms.
LncRNA W42 expression in HCC tissues and cells (Huh7 and SMMC-7721) was detected by quantitative reverse transcriptase polymerase chain reaction. After transfection with pcDNA3.1-lncRNA W42 or shRNA-lncRNA W42, cell functions were assessed by cell counting Kit-8 (CCK-8), colony formation, flow cytometry and Transwell assays. An HCC xenograft model was used to assess the role of lncRNA W42 on tumor growth in vivo. Receiver operating characteristic curves and Kaplan-Meier curves were used for clinical investigation.
LncRNA W42 expression was upregulated in HCC tissues and cells. LncRNA W42 directly bound to DBN1 and activated the downstream pathway to promote cell proliferation, and invasion of HCC. LncRNA W42 knockdown suppressed HCC xenograft tumor growth in vivo. HCC patients with high lncRNA W42 expression exhibited shorter survival times.
Upregulation of lncRNA W42 promotes tumor development by binding with DBN1 in HCC.
LncRNA W42, which is upregulated in HCC, may serve as a potential candidate prognostic biomarker and therapeutic target in HCC.