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TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK 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 in...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9501546/ https://www.ncbi.nlm.nih.gov/pubmed/36142409 http://dx.doi.org/10.3390/ijms231810496 |
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author | Biswas, Polash Kumar Kwak, Yeonjoo Kim, Aram Seok, Jaekwon Kwak, Hee Jeong Lee, Moonjung Dayem, Ahmed Abdal Song, Kwonwoo Park, Jae-Yong Park, Kyoung Sik Shin, Hyun Jin Cho, Ssang-Goo |
author_facet | Biswas, Polash Kumar Kwak, Yeonjoo Kim, Aram Seok, Jaekwon Kwak, Hee Jeong Lee, Moonjung Dayem, Ahmed Abdal Song, Kwonwoo Park, Jae-Yong Park, Kyoung Sik Shin, Hyun Jin Cho, Ssang-Goo |
author_sort | Biswas, Polash Kumar |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9501546 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95015462022-09-24 TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway Biswas, Polash Kumar Kwak, Yeonjoo Kim, Aram Seok, Jaekwon Kwak, Hee Jeong Lee, Moonjung Dayem, Ahmed Abdal Song, Kwonwoo Park, Jae-Yong Park, Kyoung Sik Shin, Hyun Jin Cho, Ssang-Goo Int J Mol Sci Article 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. MDPI 2022-09-10 /pmc/articles/PMC9501546/ /pubmed/36142409 http://dx.doi.org/10.3390/ijms231810496 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Biswas, Polash Kumar Kwak, Yeonjoo Kim, Aram Seok, Jaekwon Kwak, Hee Jeong Lee, Moonjung Dayem, Ahmed Abdal Song, Kwonwoo Park, Jae-Yong Park, Kyoung Sik Shin, Hyun Jin Cho, Ssang-Goo TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title | TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title_full | TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title_fullStr | TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title_full_unstemmed | TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title_short | TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway |
title_sort | ttyh3 modulates bladder cancer proliferation and metastasis via fgfr1/h-ras/a-raf/mek/erk pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9501546/ https://www.ncbi.nlm.nih.gov/pubmed/36142409 http://dx.doi.org/10.3390/ijms231810496 |
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