PAR2 regulates proliferation, migration of lung cancer and chemotherapy sensitivity by involving PTEN pathway.

Background: Protease-activated receptor 2 (PAR2) is associated with tumor growth and metastasis. Here we examined the functions of PAR2 on growth, migration, invasion and chemosensitivity using both lung cancer cells and human lung cancer tissue.

Methods: The effect of PAR2 on growth of lung cancer cells was examined by MTT assay. The function of PAR2 on migration and invasion of lung cancer cells was evaluated by transwell migration and matrigel invasion assays. The role of PAR2 on paclitaxel-induced apoptosis was evaluated by Caspase-Glo3/7 assay. PAR2 levels in human lung cancer tissue were measured by qRT-PCR assay.

Results: Overexpression of PAR2 increased the proliferation, promoted migration and invasion in lung cancer cells. Up-regulation of PAR2 decreased the paclitaxel treatment sensitivity in lung cancer cells. PAR2 decreased paclitaxel-induced apoptosis by regulation of BAX and Bcl-2 expression. Aberrant expression of PTEN and p-AKT in lung cancer cells was impacted by PAR2. Serum PAR2 levels were increased in lung cancer patients. PAR2 expression was higher in human lung cancer tissue than normal lung tissues and associated with cancer stage.

Conclusions: PAR2 displayed essential roles in lung carcinogenesis and might act as a potential biomarker to predict chemotherapy response and prognosis in lung cancer.