TTYH3 Modulates Bladder Cancer Proliferation and Metastasis via FGFR1/H-Ras/A-Raf/MEK/ERK Pathway.
Polash Kumar BiswasYeonjoo KwakAram KimJaekwon SeokHee Jeong KwakMoonjung LeeAhmed Abdal DayemKwonwoo SongJae-Yong ParkKyoung Sik ParkHyun Jin ShinSsang-Goo ChoPublished in: International journal of molecular sciences (2022)
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.
Keyphrases
- signaling pathway
- pi k akt
- cell proliferation
- poor prognosis
- spinal cord injury
- papillary thyroid
- single cell
- epithelial mesenchymal transition
- induced apoptosis
- cell therapy
- squamous cell carcinoma
- binding protein
- wastewater treatment
- stem cells
- squamous cell
- big data
- machine learning
- mesenchymal stem cells
- muscle invasive bladder cancer
- mass spectrometry
- long non coding rna
- endoplasmic reticulum stress
- deep learning