Suberoylanilide hydroxamic acid inhibits LX2 cells proliferation via decreasing yes-associated protein/transcriptional coactivator with PDZ-binding motif proteins
Autor: | Merve Özel, Mevlut Baskol, Eser Kilic, Gulden Baskol, Nazlı Helvacı, Kenan Güçlü |
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Přispěvatelé: | Tıp Fakültesi, Kenan Güçlü / 0000-0002-0092-652X |
Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Suberoylanilide hydroxamic acid Hippo pathway Biochemistry (medical) Clinical Biochemistry Biochemistry Cell biology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine 030220 oncology & carcinogenesis Suberoylanilide Hydroxamic Acid Transcriptional Coactivator YAP/TAZ Pdz binding motif Molecular Biology Hepatic fibrosis |
Popis: | Background Hepatic fibrosis is a complex and dynamic process similar to “wound healing” that results in the progressive accumulation of connective tissue. We aimed to investigate the epigenetic control of liver fibrosis and Hippo pathway in human hepatic stellate cell (HSC) line. We examined the effect of Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor on the LX2 cell line. Material and methods 2.5 μM SAHA was treated to LX2 cell line for 2 days. Cell proliferation and apoptosis measurement were performed by Muse Cell Analyzer. Yes-Associated Protein/Transcrıptional Coactivator With Pdz-Binding Motif (YAP/TAZ) and alpha-smooth muscle actin (α-SMA) protein expression levels were measured by western blotting. Results In our study, we observed that the SAHA treatment reduced cell viability and induced apoptosis of LX2 cells statistically. We found that SAHA treatment decreased α-SMA, YAP and TAZ proteins levels statistically. Conclusion Decreased cell viability could be due to physiological, autophagical and also related to the apoptotical mechanisms. We thought that SAHA plays an important role in the creation of the fates of the LX2 cell line. |
Databáze: | OpenAIRE |
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