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

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

doi:10.3390/ijms231810496

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

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

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16 Citations (Scopus)

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.

Original language	English
Article number	10496
Journal	International journal of molecular sciences
Volume	23
Issue number	18
DOIs	https://doi.org/10.3390/ijms231810496
Publication status	Published - 2022 Sept

Bibliographical note

Funding Information:
This paper was supported by Konkuk University in 2019.

Publisher Copyright:
© 2022 by the authors.

Keywords

FGFR1
MAPK
TTYH3
bladder cancer
gene expression
patient survival

ASJC Scopus subject areas

Catalysis
Molecular Biology
Spectroscopy
Computer Science Applications
Physical and Theoretical Chemistry
Organic Chemistry
Inorganic Chemistry

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3390/ijms231810496

Cite this

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title = "TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway",

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.",

keywords = "FGFR1, MAPK, TTYH3, bladder cancer, gene expression, patient survival",

author = "Biswas, {Polash Kumar} and Yeonjoo Kwak and Aram Kim and Jaekwon Seok and Kwak, {Hee Jeong} and Moonjung Lee and Dayem, {Ahmed Abdal} and Kwonwoo Song and Park, {Jae Yong} and Park, {Kyoung Sik} and Shin, {Hyun Jin} and Cho, {Ssang Goo}",

note = "Funding Information: This paper was supported by Konkuk University in 2019. Publisher Copyright: {\textcopyright} 2022 by the authors.",

year = "2022",

month = sep,

doi = "10.3390/ijms231810496",

language = "English",

volume = "23",

journal = "International journal of molecular sciences",

issn = "1661-6596",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

number = "18",

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AU - Biswas, Polash Kumar

AU - Kwak, Yeonjoo

AU - Kim, Aram

AU - Seok, Jaekwon

AU - Kwak, Hee Jeong

AU - Lee, Moonjung

AU - Dayem, Ahmed Abdal

AU - Song, Kwonwoo

AU - Park, Jae Yong

AU - Park, Kyoung Sik

AU - Shin, Hyun Jin

AU - Cho, Ssang Goo

PY - 2022/9

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N2 - 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.

AB - 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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KW - MAPK

KW - TTYH3

KW - bladder cancer

KW - gene expression

KW - patient survival

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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