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6,6′-Bieckol induces apoptosis and suppresses TGF-β-induced epithelial-mesenchymal transition in non-small lung cancer cells

OBJECTIVE: In this study, the aim was to investigate the inhibitory effect of 6,6′-bieckol on the migration and epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) cells, and explore its potential molecular mechanisms. METHODS: Cell migration was measured using a CCK8, woun...

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Detalles Bibliográficos
Autores principales: Li, Yongxin, Liu, Man, Yang, Kunlong, Tian, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9476679/
https://www.ncbi.nlm.nih.gov/pubmed/36117661
http://dx.doi.org/10.1016/j.chmed.2021.05.005
Descripción
Sumario:OBJECTIVE: In this study, the aim was to investigate the inhibitory effect of 6,6′-bieckol on the migration and epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) cells, and explore its potential molecular mechanisms. METHODS: Cell migration was measured using a CCK8, wound healing, and transwell migration assay. Apoptosis was determined using an Annexin V/propidium iodide staining. Western blotting and immunofluorescence were used to examine the expression level of apoptosis-related proteins and EMT marker proteins. RESULTS: The results showed that 6,6′-bieckol inhibited migration and induced apoptosis of NSCLC cells. Furthermore, 6,6′-bieckol had significantly up-regulated the E-cadherin and down-regulated Snail1 and Twist1 transcriptional levels. 6,6′-Bieckol might inhibit TGF-β-induced EMT by down-regulating Snail1 and Twist1 and up-regulating E-cadherin in lung cancer cells. CONCLUSION: It is suggested that 6,6′-bieckol has the potential to be developed as a therapeutic candidate for lung cancer.