Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Cong Cheng
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Yi xiang Liao
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Li Wang
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Jin min Zeng
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Fang fang Zhou
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Xiu qin Zhang
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China
Tao Yang
Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China; The Second Clinical Medical College to Yangtze University, Jing Zhou City 434020, Hubei Province, PR China; Corresponding author. Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China .
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.
