HLA complex group 11 is involved in colorectal carcinoma cisplatin resistance via the miR‑214‑5p/SOX4 axis

Xie,Jianping; Zhu,Jiaping; Pang,Jie; Ma,Yaping

doi:10.3892/ol.2021.12796

HLA complex group 11 is involved in colorectal carcinoma cisplatin resistance via the miR‑214‑5p/SOX4 axis

Authors:
- Jianping Xie
- Jiaping Zhu
- Jie Pang
- Yaping Ma
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Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Yangtze University, The First People's Hospital of Jingzhou, Jingzhou, Hubei 434000, P.R. China, Department of Clinical Laboratory, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang Central Hospital, Xiangyang, Hubei 441000, P.R. China
Published online on: May 19, 2021 https://doi.org/10.3892/ol.2021.12796
Article Number: 535
Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the roles and potential mechanisms of long non‑coding RNA HLA complex group 11 (HCG11) in colorectal carcinoma. Reverse transcription‑quantitative PCR was used to detect HCG11 expression in clinical tissues and survival analysis was performed to identify its prognostic value. In order to investigate its specific biological functions in colorectal carcinoma, the transfection technique was used for the knockdown and overexpression of HCG11. Dual‑luciferase reporter gene and RNA pull‑down assays were used to identify the binding association between HCG11 and microRNA (miR)‑214‑5p. Western blot analysis was used to detect the mechanism of epithelial‑mesenchymal transition (EMT) regulation in tumor cells in the pathway downstream of HCG11. HCG11 level was high in colorectal carcinoma tissues, which was associated with poor patient prognosis; however, chemotherapy may prevent the upregulation of HCG11 in colorectal carcinoma. HCG11‑knockdown suppressed the proliferation, migration and chemotherapeutic sensitivity of colorectal carcinoma cells, whereas HCG11‑overexpression enhanced chemotherapeutic sensitivity. miR‑214‑5p was revealed to be a target gene, and upon direct interaction, a negative regulator of HCG11 in colorectal carcinoma cells. Inhibition of miR‑214‑5p reversed the restriction of HCG11 on the malignant activity of colorectal carcinoma cells, while miR‑214‑5p mediated the chemotherapy‑related intracellular EMT pathway. In conclusion, HCG11 is a vital oncogene of colorectal carcinoma involved in mediating the chemotherapeutic resistance of tumors.

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