VDAC1型
癌症研究
基因敲除
癌变
生物
癌症
细胞凋亡
生物化学
遗传学
基因
细菌外膜
大肠杆菌
作者
Hongyan Xiao,Lijun Ma,Jie Ding,Honghong Wang,Xiaofang Bi,Fengmei Tan,Wenhua Piao
出处
期刊:Current Cancer Drug Targets
[Bentham Science]
日期:2024-03-01
卷期号:24 (3): 354-367
被引量:1
标识
DOI:10.2174/1568009624666230912095526
摘要
Although endometrial cancer represents a frequently diagnosed malignancy of the female reproductive tract, we know very little about the factors that control endometrial cancer.Our study was presented to investigate the function of MCU in endometrial tumorigenesis and the molecular mechanisms involved.A total of 94 endometrial cancer patients were recruited into our cohort. MCU and VDAC1 expression was examined in tumor and normal tissues via immunohistochemistry and immunofluorescence. Associations of MCU and VDAC1 expression with clinicopathological characteristics were evaluated. After transfection with shRNA targeting MCU or full-length MCU plasmids, clone formation, wound healing, transwell and MitoTracker Red staining were separately presented in Ishikawa and RL95-2 cells. Moreover, Western blotting or immunofluorescence was utilized to examine the expression of MCU, VDAC1, Na+/Ca2+/Li+ exchanger (NCLX), and β-catenin under VDAC1 knockdown and/or MCU overexpression or knockdown.MCU and VDAC1 expression were prominently up-regulated in endometrial cancer tissues and were significantly associated with histological grade, depth of myometrial invasion and lymph node status. MCU up-regulation enhanced clone formation, migration, and mitochondrial activity of endometrial cancer cells. The opposite results were investigated when MCU was silenced. MCU or VDAC1 silencing reduced the expression of MCU, VDAC1, NCLX, and β-catenin. Moreover, VDAC1 knockdown alleviated the promoting effect of MCU overexpression on the above proteins.This investigation demonstrated that MCU-induced mitochondrial calcium uptake plays a critical role in endometrial tumorigenesis through interaction with VDAC1.
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