Xie Jianping, Zhu Jiaping, Pang Jie, Ma Yaping
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.
Oncol Lett. 2021 Jul;22(1):535. doi: 10.3892/ol.2021.12796. Epub 2021 May 19.
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.
本研究旨在探讨长链非编码RNA HLA复合体基因座11（HCG11）在结直肠癌中的作用及潜在机制。采用逆转录定量PCR检测临床组织中HCG11的表达，并进行生存分析以确定其预后价值。为了研究其在结直肠癌中的具体生物学功能，采用转染技术对HCG11进行敲低和过表达。采用双荧光素酶报告基因和RNA下拉实验鉴定HCG11与微小RNA（miR）-214-5p之间的结合关系。采用蛋白质免疫印迹分析检测HCG11下游通路中肿瘤细胞上皮-间质转化（EMT）调控机制。结直肠癌组织中HCG11水平较高，这与患者预后不良相关；然而，化疗可能会阻止结直肠癌中HCG11的上调。敲低HCG11可抑制结直肠癌细胞的增殖、迁移和化疗敏感性，而过表达HCG11则增强化疗敏感性。miR-214-5p被证实为一个靶基因，直接相互作用时，它是结直肠癌细胞中HCG11的负调控因子。抑制miR-214-5p可逆转HCG11对结直肠癌细胞恶性活性的限制，而miR-214-5p介导化疗相关的细胞内EMT通路。总之，HCG11是结直肠癌的一个重要癌基因，参与介导肿瘤的化疗耐药性。
