Long non‑coding RNA LINC00173 enhances cisplatin resistance in hepatocellular carcinoma via the microRNA‑641/RAB14 axis
- Guangliang Zhao
- Anhua Zhang
- Shufang Sun
- Yunlong Ding
Affiliations: Department of Emergency General Surgery, Weifang People's Hospital, Weifang, Shandong 261000, P.R. China, Department of Gastrointestinal Surgery, Gaomi People's Hospital, Gaomi, Shandong 261500, P.R. China, Department of Anesthesia, Weifang Maternal and Child Health Hospital, Weifang, Shandong 261000, P.R. China
- Published online on: March 13, 2021 https://doi.org/10.3892/ol.2021.12632
Copyright: © Zhao
et al. This is an open access article distributed under the
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A growing body of evidence indicates that long non‑coding RNAs (lncRNAs) play crucial roles in the chemoresistance of human cancers. However, the molecular mechanisms underlying the functions of certain lncRNAs in the chemotherapeutic resistance of hepatocellular carcinoma (HCC) remain unclear. The aim of the present study was to investigate the function and potential mechanism of action of lncRNA LINC00173 in HCC cisplatin (DDP) resistance. Reverse transcription‑quantitative PCR analysis indicated that LINC00173 was highly expressed in DDP‑resistant HCC tissues and cell lines, and high expression levels of LINC00173 were found to be associated with poor prognosis in patients with HCC. Moreover, LINC00173‑knockdown improved the DDP sensitivity of DDP‑resistant HCC cells. A luciferase reporter assay also demonstrated that microRNA (miR)‑641 was a direct target of LINC00173. miR‑641 inhibition restored the promoting effect of LINC00173 knockdown on DDP sensitivity in HCC cells. Furthermore, RAB14 was identified as a target of miR‑641, and RAB14 overexpression restrained the inducing effect of LINC00173 knockdown on HCC cell DDP sensitivity. The findings of the present study demonstrated that LINC00173 increased DDP resistance in HCC via the miR‑641/RAB14 axis, which may represent a promising therapeutic strategy for HCC.