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TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathwayopen access

Authors
Biswas, Polash KumarKwak, YeonjooKim, AramSeok, JaekwonKwak, Hee JeongLee, MoonjungDayem, Ahmed AbdalSong, KwonwooPark, Jae-YongPark, Kyoung SikShin, Hyun JinCho, Ssang-Goo
Issue Date
9월-2022
Publisher
MDPI
Keywords
bladder cancer; FGFR1; gene expression; MAPK; patient survival; TTYH3
Citation
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, no.18
Indexed
SCIE
SCOPUS
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume
23
Number
18
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/145818
DOI
10.3390/ijms231810496
ISSN
1661-6596
Abstract
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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