FRA-1 can promote motility, invasion, and anchorage-independent growth of lung epithelial cells in vitro, but is insufficient for tumor formation

Data suggest that Fra-1 enhances lung cancer epithelial cell motility and invasion by inducing the activity of matrix metalloproteinases, in particular MMP-2 and MMP-9, and EGFR-activated signaling.

Results suggest that Fra-1 is upregulated in lung cancer tissues and functions by affecting the P53 signaling pathway.

High FOS-like antigen 1 (FOSL1) expression with mutant KRAS protein lung and pancreatic cancer patients showed the worst survival outcome.

FOSL1 is a determinant of lung cancer in vivo and regulates tumor cell proliferation and survival, largely in the context of KRAS mutations through amphiregulin and cell survival gene regulation.