MicroRNA-1179 suppresses the proliferation and enhances vincristine sensitivity of oral cancer cells via induction of apoptosis and modulation of MEK/ERK and PI3K/AKT signalling pathways.

The role of miR-1179 in the development of cancer has been proved by different studies. However, the expression profile and role of miR-1179 is yet to be explored in human oral cancer. Consistently, this study was undertaken to explore the molecular role of miR-1179 in regulation of the human oral cancer development and progression. The results showed miR-1179 to be significantly (p < 0.05) overexpressed in all the oral cancer cell lines relative to normal cells. The repression of miR-1179 transcript levels not only suppressed the proliferation of oral cancer cells but also increased their sensitivity to vincristine. The decline in proliferative rates was attributed to induction of autophagy in oral cancer cells as confirmed by transmission electron microscopic analysis. Western blot analysis showed that the expression of LC3B-II increased and that of beclin 1 decreased while LC3B-I expression remained constant upon miR-1179 inhibition. Inhibition of miR-1179 caused significant decrease in the migration and invasion of the oral cancer cells. The migration and invasion found to be 47% and 32% for SCC-9 and 24% and 28% for SCC-25 cells upon miR-1179 inhibition. At molecular level, the miR-1179 was shown to exert its anticancer effects via deactivation of MEK/ERK and PI3K/AKT signalling cascades. In conclusion, the findings point towards the potential of miR-1179 in the treatment of oral cancer.