Overexpression of long non‑coding RNA cancer susceptibility 11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Liu,Haidong; Liu,Tao; Zhou,Yong; Song,Xinwen; Wei,Rendong

doi:10.3892/ol.2020.11265

Overexpression of long non‑coding RNA cancer susceptibility 11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Authors:
- Haidong Liu
- Tao Liu
- Yong Zhou
- Xinwen Song
- Rendong Wei
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Affiliations: Department of Digestive Diseases, The Sixth People's Hospital of Qingdao, Qingdao, Shandong 266033, P.R. China, Department of Hepatology, The Sixth People's Hospital of Qingdao, Qingdao, Shandong 266033, P.R. China, Department of Infectious Diseases, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China
Published online on: January 8, 2020 https://doi.org/10.3892/ol.2020.11265
Pages: 1993-1998

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Abstract

The long non‑coding (lnc)RNA cancer susceptibility 11 (CASC11) promotes gastric cancer, however its role in other diseases is unknown. The present study demonstrated upregulation of lncRNA CASC11 and microRNA (miR)‑21 in hepatocellular carcinoma (HCC). Furthermore, the expression of CASC11 was positively correlated with that of miR‑21 in HCC tumors. Moreover, overexpression of lncRNA CASC11 led to upregulation of miR‑21 in HCC cells, whereas overexpression of miR‑21 had no effect on CASC11 levels. The levels of lncRNA CASC11 and miR‑21 were found to be upregulated in the plasma of patients with HCC during chemotherapy. In vitro cell experiments demonstrated upregulation of lncRNA CASC11 in HCC cells treated with carboplatin. Additionally, overexpression of lncRNA CASC11 promoted, whereas its knockdown inhibited the viability of HCC cells following carboplatin treatment. Finally, overexpression of miR‑21 ameliorated the effects of lncRNA CASC11 knockdown on cell viability. Thus, these findings suggest that upregulation of lncRNA CASC11 is involved in the development of chemoresistance to carboplatin in patients with HCC, via the upregulation of miR‑21.

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