FRS2 promotes the progression of non-small cell lung cancer

Lung cancer is one of the leading causes for cancer mortality worldwide, and non-small cell lung cancer (NSCLC) accounts for the majority of all lung cancer cases. FRS2 is a member of the adaptor protein family that binds receptor tyrosine kinases, and is essential for the signaling cascades mediated by FGFR. In this study, we focused our research on the function of FRS2 in NSCLC, which has not been reported before. We found that FRS2 was upregulated in NSCLC tissues, and the expression levels of FRS2 in NSCLC were correlated with advanced stage, poor differentiation, and lymph node metastasis. Knockdown of FRS2 inhibited cell proliferation, migration and invasion in NSCLC cells lines. Importantly, knockdown of FRS2 inhibited ERK1/2 signaling in NSCLC cells, suggesting that FRS2 could affect NSCLC progression through the ERK1/2 signaling pathway.