Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

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

Jirong Zhang, Yong Pan, Dehua Liao, Jingyi Tang, Dunwu Yao

Department of Pharmacy, Hunan Provincial Tumor Hospital, Changsha 410006, China;

For correspondence:- Dunwu Yao Email: yaodunwumedchs@163.com

Accepted: 27 June 2018 Published: 28 July 2018

Citation: Zhang J, Pan Y, Liao D, Tang J, Yao D. Peptide 17, an inhibitor of YAP/TEAD4 pathway, mitigates lung cancer malignancy. Trop J Pharm Res 2018; 17(7):1255-1262 doi: 10.4314/tjpr.v17i7.5

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: Lung cancer, Yes-associate protein, Transcriptional enhancer activation domain 4 (TEAD4), Peptide 17, Apoptosis