Abstract
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.
Highlights
Despite advancement in science and technology, the current strategies employed for the treatment of human oral cancer are still far from descent
MiR‐1179 inhibition suppresses the proliferation and enhances chemosensitivity of oral cancer cells To reveal the molecular functionality of miR-1179 in oral cancer, the suppression of miR-1179 was achieved by transfecting the SCC-9 and SCC-25 cancer cells with miR-1179 inhibitor
Using miR-NC transfected as control, the repression of miR-1179 transcript levels was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) method which showed significant (p < 0.05) decrease of miR-1179 expression in SCC-9 and SCC-25 cells (Fig. 1b) the results showed that suppression of miR-1179 resulted in remarkable decline of proliferation rates of SCC-9 and SCC-25 cancer cells (Fig. 1c)
Summary
Despite advancement in science and technology, the current strategies employed for the treatment of human oral cancer are still far from descent. The survival rates of oral cancer are comparatively lower than breast and prostate cancers. The miRs have been shown to regulate the proliferation of human cancers but have been shown to have influence the metastasis to neighbouring tissues (Peng et al 2011). MicroRNA-1179 (miR-1179) has been implicated in the regulation of proliferation and metastasis of different human cancers (Jiang et al 2015, Krutovskikh et al 2010, Song et al 2018, Lin et al 2018). The inhibition of metastasis of hepatocellular carcinoma has been reported to be due to interaction of miR-365 with ZEB2 (Gao et al 2019). This study was designed to investigate the role of miR-1179 in human oral cancer cells via modulation of the MEK/ERK and PI3K/AKT signalling pathways
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