Lung cancer is the leading cause of cancer-related death in men and women with a 5-year survival rate of 18%. The PI3K/Akt pathway plays a role in non-small cell lung cancer tumorigenesis and progression. FCH domain only 1(FCHO1) is overexpressed in lung cancer and promotes entry into mitosis and G1/S phase transition, leading to cancer cell growth. Our group has investigated the relationship between FCHO1 and the Akt signaling pathway, which plays an important role in lung cancer growth. Serine 570 of human FCHO1, a part of the Akt kinase motif, was known to be phosphorylated by Akt. To inhibit FCHO1 phosphorylation, we developed the FCHO1560-571 peptide. FCHO1560-571 peptide exhibits higher binding affinity to Akt and inhibits lung cancer cell proliferation. Moreover, the FCHO1560-571 peptide significantly decreased p-Akt, p-ERK and CDC2 levels. These results suggest that the FCHO1560-571 peptide inhibits cancer progression through the Akt/ERK/CDC2 pathway.
There are few studies investigating the function of FCHO1 in cancer cell growth. In this mini review, we summarize recent articles on the role of FCHO1 in lung cancer progression. The reviewed articles suggest that inhibition of FCHO1 activity through the regulation of Akt signaling could be developed as a novel lung cancer treatment.
Lung cancer, Akt signaling pathway, FCHO1, Cell cycle, Midbody