| 引用本文： |
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方子祥,王益富,沈甫明,等.RCOR1在食管癌中的表达与功能研究[J].同济大学学报（医学版）,2023,44(1):7-14. [点击复制]
- FANG Zixiang,WANG Yifu,SHEN Fuming,et al.Expression level and role of RCOR1 in esophageal carcinoma[J].Journal of Tongji University(Medical Science),2023,44(1):7-14. [点击复制]
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| 摘要: |
| 目的探讨REST辅助转录抑制因子(repressor element-1 silencing transcription factor corepressor 1, RCOR1/CoREST)在食管癌(esophageal carcinoma, EC)中的表达水平和生物学功能。方法通过癌症基因数据库(TCGA)数据分析RCOR1在肿瘤与正常组织中的表达水平及与EC患者预后的关系。通过qPCR检测RCOR1在EC和正常组织中的mRNA表达量，通过Western印迹法检测正常食管上皮细胞与EC细胞中RCOR1蛋白表达水平。在EC细胞(EC109和EC9706)中转染siRNA敲减RCOR1表达，慢病毒感染EC109和EC9706过表达RCOR1，使用qPCR和Western印迹法检测敲减和过表达效率。通过CCK8和克隆形成实验检测细胞增殖能力，流式细胞术检测细胞凋亡，通过细胞迁移实验检测细胞迁移能力，通过裸鼠皮下成瘤实验检测细胞体内成瘤能力。结果与正常组织和正常食管上皮细胞相比，RCOR1在EC组织及细胞中均呈显著高表达，同时TCGA数据库分析表明RCOR1高表达EC患者预后较差。敲减RCOR1表达明显减弱EC细胞的增殖能力、克隆形成能力和细胞迁移能力，并诱导EC细胞发生凋亡，体内实验结果表明RCOR1敲减后减弱EC细胞体内成瘤能力。结论RCOR1在EC中发挥癌基因的功能，促进EC细胞的生长及增殖。 |
| 关键词: RCOR1 食管癌 癌基因 细胞增殖 |
| DOI：10.12289/j.issn.1008-0392.22141 |
| 通信作者: |
| 投稿时间：2022-04-09 |
| 录用日期： |
| 基金项目:上海市卫健委协同创新集群(2019CXJQ03) |
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| Expression level and role of RCOR1 in esophageal carcinoma |
| FANG Zixiang,WANG Yifu,SHEN Fuming,WANG Aiping |
| (Hengyang Medical College, University of South China, Hengyang 421001, Hunan Province, China;Department of Pharmacy, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai 200072, China) |
| Abstract: |
| ObjectiveTo investigate the expression and role of RCOR1 in esophageal carcinoma(EC). MethodsThe expression of RCOR1 in tumor and normal tissue and its relationship with the prognosis of patients with EC was analyzed by using TCGA database. The mRNA expression level of RCOR1 in EC and normal tissues was detected by qPCR assay, and the protein expression level of RCOR1 in normal esophageal epithelial cells and EC cells was detected by Western blot（WB）. The expression of RCOR1 in EC cell lines EC109 and EC9706 was knocked down by RCOR1-siRNA；EC109 and EC9706 cells were transfected with lentivirus-mediated vectors to over-express RCOR1. The knockdown and overexpression efficiency were detected by qPCR and WB, respectively. CCK8 and colony formation assays were used to determine cell proliferation and colony formation; flow cytometry was used to analyze cell apoptosis; Transwell assay was used to determine the cell migration. The effects of preprocessed EC cells in vivo were detected by xenograft tumors assay. ResultsCompared with normal tissues and normal esophageal epithelial cells, the expression of RCOR1 was higher in EC tissues and cells. TCGA database analysis showed poor prognosis in EC patients with high RCOR1 expression. The knockdown of RCOR1 significantly reduced the proliferation, clone formation and migration ability of EC cells, and induced the apoptosis of EC cells. Results of xenograft tumors assay showed that knockdown of RCOR1 attenuated the tumorigenic ability of EC cells in vivo. ConclusionRCOR1 promotes the proliferation of EC cells and may act as an oncogene in EC. |
| Key words: RCOR1 esophageal carcinoma oncogene cell proliferation |
