Abstract
This study assessed the biological functions of LIM-domain-only 4 (LMO4) in gastric cancer (GC) and investigated the underlying molecular mechanisms. It was found that the expression of LMO4 was significantly upregulated in GC tissues and closely associated with clinicopathological factors, overall survival and disease-free survival of patients. After knockdown of LMO4 in MGC-803 and SGC-7901 cells, invasion and proliferation were obviously suppressed. Furthermore, LMO4 knockdown suppressed the phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt and mammalian target of rapamycin (mTOR). Miltefosine, the inhibitor of PI3K/Akt, and dactolisib, the inhibitor of mTOR, abrogated recombinant LMO4-induced GC cell invasion and proliferation. These results suggest that LMO4 promotes GC cell invasion and proliferation mainly through PI3K-Akt-mTOR signaling. LMO4 may serve as a potential therapeutic target for GC in the future.