Abstract
Background: The function of TMEM176A in human lung cancer remains to be elucidated. Materials & Methods: Nine cell lines and 123 cases of lung cancers were employed. Results: TMEM176A was highly expressed in H727 cells, reduced expression was observed in A549, H446 and H460 cells, loss of expression was found in H157, H1563, H358, H1299 and H23 cells. TMEM176A was unmethylated in H727 cells, partially methylated in A549, H446 and H460 cells, and fully methylated in H157, H1563, H358, H1299 and H23 cells. Loss of/reduced expression of TMEM176A is correlated to promoter region methylation. Restoration of TMEM176A expression was induced by 5-AZA-2- deoxycytidine in complete methylated cells, increased expression of TMEM176A was observed in partially methylated cells. These results suggest that TMEM176A is regulated by promoter region methylation in lung cancer cells. TMEM176A was methylated in 53.66% (66/123) of non-small cell lung cancers (NSCLCs) samples. Reduced expression of TMEM176A was associated with promoter region methylation in 40 cases of matched primary NSCLCs and adjacent tissue samples (P<0.05). TMEM176A expression induced cell apoptosis, inhibited colony formation, cell proliferation, migration and invasion. Conclusion: Methylation of TMEM176A activated ERK signaling in lung cancer cells. TMEM176A suppressed human lung cancer cell xenograft growth in mice.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
