Abstract 699: KMT2A regulates cervical cancer cell growth andapoptosisthrough cooperation with VDAC1

Abstract

Abstract Cervical cancer is an aggressive cutaneous malignancy, illuminating the exact mechanisms of tumorigenesis and discovering novel therapeutic targets are urgently needed. Lysine methyltransferase 2A (KMT2A) is a transcriptional co-activator regulating gene expression during early development and hematopoiesis, but the role of KMT2A in cervical cancer remains largely unknown. Here, we showed that KMT2A regulated cervical cancer cell growth and apoptosis through cooperation with VDAC1 (voltage dependent anion channel 1). Knockdown of KMT2A significantly inhibited cell viability and cell migration and induced apoptosis in cervical cancer cells. Overexpression of VADC1 reversed the KMT2A knockdown-mediated suppression of cell viability and cell migration and induction of apoptosis. The results from a xenograft mouse model confirmed that KMT2A regulated cervical cancer growth via the VDAC1 signaling. Moreover, analyses of clinical samples demonstrated that the expression of KMT2A and VDAC1 were positively correlated in cervical cancer tissues, especially in cervical intraepithelial neoplasia (CIN) samples. Collectively, our results indicated that KMT2A promoted cervical cancer growth by cooperating with the VDAC1, suggesting that the KMT2A/VDAC1 signaling pathway may be a potential therapeutic target for cervical cancer. Citation Format: Changlin Zhang, Yizhuo Li, Qian Long, Tianze Liu, Ge Qin, Dingbo Shi, Miao Chen, Kefang Zhang, Shuihan Shi, Wuguo Deng. KMT2A regulates cervical cancer cell growth andapoptosisthrough cooperation with VDAC1 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 699.