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 ...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.展开更多
基金supported by the National Natural Science Foundation of China(81774228,31972171,31671944)Natural Science Foundation by Xuzhou City(KC21160)the PAPD of Jiangsu Higher Education Institutions,and Scientific Research Support Project for Teachers with Doctor’s Degrees(Jiangsu Normal University,17XLR034)。
文摘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.
