Peptide 17, an inhibitor of YAP/TEAD4 pathway, mitigates lung cancer malignancy

Abstract

Purpose: To investigate whether and how peptide 17 affects lung cancer cells. Methods: Human lung carcinoma cells, LLC and PC-9, were employed to study the therapeutic effect of peptide 17 on lung cancer. After exogenous expression of peptide 17, a co-immunoprecipitation experiment was used to examine the inhibitory effect of peptide 17. CCK8 assay was employed to assess the lung cancer cells’ viability while clone formation assays were used to assess lung cancer cell proliferation. Colony number was also determined. The stimulatory effect of peptide 17 on lung cancer cell apoptosis was assessed by fluorescence-activated cell sorting (FACS). Results: Peptide 17 efficiently disrupted the interaction between YAP and TEAD4 (p < 0.001), and decreased the expression of CTGF and Cyr61. In addition, lung cancer cell viability and proliferation significantly decreased (p < 0.001) in a time- and concentration-dependent manner. On the other hand, the proportion of apoptotic cells was significantly elevated with rising concentration of peptide 17. Conclusion: Exogenous expression of peptide 17 activates Bcl2/Bax/caspase-9 signal and is responsible for its inhibitory effects on lung cancer cells. Thus, peptide 17 is a promising target drug in lung cancer treatment.