KMT2A regulates cervical cancer cell growth through targeting VDAC1
Changlin Zhang, Yi‐Jun Hua, Huijuan Qiu, Tianze Liu, Long Qian, Wei Liao, Jiehong Qiu, Nang Wang, Miao Chen, Dingbo Shi, Yue Yan, Chuanbo Xie, Wuguo Deng, Tian Li, Yizhuo Li
Abstract
results from a cervical cancer xenograft mouse model also validated that KMT2A knockdown suppressed tumor growth by inhibiting VDAC1, whereas KMT2A overexpression promoted cervical cancer growth. Moreover, analyses of Biewenga cervix database and clinical samples showed that both KMT2A and VDAC1 were upregulated in cervix squamous cell carcinoma compared with cervix uteri tissues, and their expression was negatively correlated with the differentiation grade of cervical cancer. Our results therefore indicated that the KMT2A/VDAC1 signaling axis may be a potential new mechanism of cervical carcinogenesis.