Epigenetic regulation of FOXI2 promotes clear cell renal cell carcinoma progression

被引:0
|
作者
Zhou, Shuai [1 ,2 ]
Cheng, Cong [1 ,2 ]
Liao, Yi Xiang [1 ,2 ]
Wang, Li [1 ,2 ]
Zeng, Jin Min [1 ,2 ]
Zhou, Fang Fang [1 ,2 ]
Zhang, Xiu Qin [1 ,2 ]
Yang, Tao [1 ,2 ]
机构
[1] Yangtze Univ, Jing Zhou Hosp Affiliated, Dept Urol, Jingzhou, Peoples R China
[2] Yangtze Univ, Clin Med Coll 2, Jingzhou 434020, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
FOXI2; Methylation; Renal cancer; Cell cycle arrest; METHYLATION; HYPERMETHYLATION; CLASSIFICATION; SURVIVAL; GENOMICS;
D O I
10.1016/j.heliyon.2024.e29218
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In recent decades, substantial advancements in epigenetics have unveiled a profound understanding of its mechanisms in tumorigenesis and have offered promising strategies for epigenetic therapy in cancer patients. In our study, through bioinformatics analysis, we discovered a significant downregulation and hypermethylation of FOXI2 in clear cell renal cell carcinoma (ccRCC), while the expression in chromophobe cell carcinoma (chRCC) exhibited the opposite trend. Moreover, we established a strong correlation between FOXI2 expression levels and the prognosis of ccRCC. Gene enrichment analysis and cell function experiments unequivocally demonstrate that FOXI2 possesses the capability to induce cell cycle arrest and inhibit cell proliferation. Our research findings demonstrate that the expression of FOXI2 in ccRCC is under the regulation of promoter hypermethylation. Furthermore, in vitro experiments have conclusively shown that the overexpression of FOXI2 induces cell cycle arrest and inhibits cell proliferation.
引用
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页数:10
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