基因敲除
癌症研究
膀胱癌
MAPK/ERK通路
细胞生长
癌症
转移
下调和上调
信号转导
成纤维细胞生长因子受体1
癌细胞
细胞
生物
医学
化学
细胞培养
细胞生物学
成纤维细胞生长因子
内科学
受体
基因
生物化学
遗传学
作者
Polash Kumar Biswas,Yeonjoo Kwak,Aram Kim,Jaekwon Seok,Hee Jeong Kwak,Moonjung Lee,Ahmed Abdal Dayem,Kwonwoo Song,Jae Yong Park,Kyoung Sik Park,Hyun Jin Shin,Ssang-Goo Cho
标识
DOI:10.3390/ijms231810496
摘要
Tweety family member 3 (TTYH3) is a calcium-activated chloride channel with a non-pore-forming structure that controls cell volume and signal transduction. We investigated the role of TTYH3 as a cancer-promoting factor in bladder cancer. The mRNA expression of TTYH3 in bladder cancer patients was investigated using various bioinformatics databases. The results demonstrated that the increasingly greater expression of TTYH3 increasingly worsened the prognosis of patients with bladder cancer. TTYH3 knockdown bladder cancer cell lines were constructed by their various cancer properties measured. TTYH3 knockdown significantly reduced cell proliferation and sphere formation. Cell migration and invasion were also significantly reduced in knockdown bladder cancer cells, compared to normal bladder cancer cells. The knockdown of TTYH3 led to the downregulation of H-Ras/A-Raf/MEK/ERK signaling by inhibiting fibroblast growth factor receptor 1 (FGFR1) phosphorylation. This signaling pathway also attenuated the expression of c-Jun and c-Fos. The findings implicate TTYH3 as a potential factor regulating the properties of bladder cancer and as a therapeutic target.
科研通智能强力驱动
Strongly Powered by AbleSci AI