Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 18, Pages -Publisher
MDPI
DOI: 10.3390/ijms231810496
Keywords
bladder cancer; FGFR1; gene expression; MAPK; patient survival; TTYH3
Funding
- Konkuk University
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This study investigated the role of TTYH3 in bladder cancer and found that high expression of TTYH3 was associated with poor prognosis in bladder cancer patients. Knockdown of TTYH3 in bladder cancer cells resulted in significantly reduced cell proliferation, sphere formation, migration, and invasion, possibly through the downregulation of FGFR1 phosphorylation and subsequent inhibition of the H-Ras/A-Raf/MEK/ERK signaling pathway.
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.
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