Fang Ru, Xia Qiuyuan, Sun Jing, Ng Hao Zha, Liang Yan, Wang Xiaotong, Wang Xuan, Ma Henghui, Zhou Xiaojun, Cheng Yang, Rao Qiu
Department of Pathology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210002, Jiangsu, China.
Department of Medical Oncology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
J Cancer. 2019 Aug 28;10(21):5256-5263. doi: 10.7150/jca.30098. eCollection 2019.
Although the inactivation of plays oncogenic roles in tumorigenesis, regulation mechanism is rarely studied in clear cell renal cell carcinoma (RCC). Thus, we aimed to investigate the mechanism of inactivation and explore the tumor suppressing roles of in the development of clear cell RCC. We verified that hypermethylation of the promoter was correlated with decreased expression of by multi-omics analysis based on the TCGA database. This result was further confirmed in our own tumor tissues. Moreover, inhibited the ability of proliferation and invasion of RCC cells . Consistent with this, overexpressing virtually inhibited the xenograft tumor growth of ACHN cells . Finally we found that promoted cell apoptosis and cellular cycle arrest in G2/M. In conclusion, our study confirms that the hypermethylation of promoters plays oncogenic roles by the transcription inhibition of in RCC, and the tumor suppressor gene inhibits RCC cell vitality and
虽然[基因名称]的失活在肿瘤发生中起致癌作用,但在透明细胞肾细胞癌(RCC)中其调控机制鲜有研究。因此,我们旨在研究[基因名称]失活的机制,并探索[基因名称]在透明细胞RCC发生发展中的肿瘤抑制作用。基于TCGA数据库的多组学分析,我们证实了[基因名称]启动子的高甲基化与[基因名称]表达降低相关。这一结果在我们自己的肿瘤组织中得到了进一步证实。此外,[基因名称]抑制了RCC细胞的增殖和侵袭能力。与此一致,[基因名称]过表达实际上抑制了ACHN细胞的异种移植肿瘤生长。最后我们发现[基因名称]促进细胞凋亡并使细胞周期停滞在G2/M期。总之,我们的研究证实,[基因名称]启动子的高甲基化通过转录抑制[基因名称]在RCC中发挥致癌作用,肿瘤抑制基因[基因名称]抑制RCC细胞活力,并且