Abstract
Purpose: Curcumin has been shown to inhibit HNSCC cell proliferation through the AKT/MTOR pathway. We wanted to study the biological effects of curcumin‐induced AKT/MTOR inhibition in HNSCC.
Procedures: Soluble proteins (pS6, p4EBP1, FGF2 and MMP‐9) extracted from cells treated with or without 20µM curcumin overnight were analyzed by western blot. Cell motility with and without 5, 10, and 20µM curcumin was determined by transwell migration assay and compared using one‐way ANOVA in four HNSCC cell lines (FaDu, PCI15A, SCC40 and SCC066).
Results: We used the highly invasive SCC cell line PCI15a to investigate the effects of curcumin on the AKT/MTOR pathway in vitro. Phosphorylated S6 (pS6) and p4EBP1 were inhibited in cells treated with 20µM curcumin for 24 hours. Curcumin inhibited the downstream effector FGF2 by 80% in SCC40 and completely abrogated the downstream effector MMP‐9 in the PCI15a cell line. Compared to vehicle, curcumin significantly inhibited migration of the HNSCC cell lines in the transwell migration model. A significant dose‐response was found among the four curcumin concentrations for all four cell lines compared to vehicle (p<0.001).
Conclusions: Curcumin inhibits migration of HNSCC cell lines trough the AKT/MTOR pathway and its downstream targets. Cancer cell migration is a highly regulated process that permits dissemination from the primary tumor. Concentrations that inhibited cell proliferation through inhibition of AKT/MTOR and its downstream target MMP‐9 were sufficient to inhibit the invasion of a variety of HNSCC cell lines in vitro. This sensitivity of HNSCC cells to retardation of cell migration by curcumin further highlights its chemopreventive properties.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):A76.
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