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

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.

CircFOXM1 promotes proliferation and metastasis of hepatocellular carcinoma via regulating miR-1179/SPAG5 axis

“…Meanwhile, studies have also confirmed that miR-1179 can target HMGB1 to inhibit the proliferation of gastric cancer cells 24 . It has also been pointed out that miR-1179 can target the E2F5 gene in regulating pancreatic cancer cell proliferation, thereby inhibiting tumor cell migration and invasion 25 ; plays an important role in regulating the proliferation of glioblastoma cells by directly targeting E2F transcription factor 5 26 ; and plays important role in cancer through Akt signaling 27 , 28 . Moreover, circFOXM1 has been confirmed to accelerate the progression of papillary thyroid carcinoma by sponging miR-1179 10 .…”

Circular RNA circ_0062389 modulates papillary thyroid carcinoma progression via the miR-1179/high mobility group box 1 axis

“…For example, in cervical cancer, circ_0084927 can adsorb miR-1179 to regulate CDK2 expression, promote cell proliferation and inhibit apoptosis [22]. MiR-1179 expression is markedly declined in oral cancer, and it can inhibit cell proliferation, enhance vincristine sensitivity and induce apoptosis by regulating MEK/ ERK and PI3K/AKT signaling pathways [12]. In gastric cancer, miR-1179 restrains cell proliferation by targeting HMGB1 15 .…”

“…Many miRNAs, as reported, are involved in PTC progression, such as miR-224-5p, miR-188-5p and miR-451a [9][10][11]. In addition, miR-1179 can affect the progression of various tumors, such as oral cancer, gastric cancer and breast cancer [12][13][14]. In PTC, miR-1179 can target HMGB1 or ABCA9 to inhibit PTC progressions [15,16].…”

Interspecies chimeric conditions affect the developmental rate of human pluripotent stem cells

“…While we leave the determination of mechanisms responsible for regulating the developmental clock to future work, comparisons of accelerated genes with curated gene sets allowed us to speculate on candidate pathways and transcription factors/miRNAs that may be involved [40][41][42][43][44][45][46][47][48]. Enrichment of the differences between up-trend/peak times (see Materials and Methods) identified signaling pathways activated earlier in both H10 and in M100 compared to H100 samples, including G-protein coupled receptor (GPCR) signaling pathways and miRNA-regulated pathways MAPK/ERK (MIR4801, MIR4731) [49,50], and PI3K/AKT [51,52], which may play roles driving developmental rates (S11 Fig and S3 Data). We also identified developmental regulators of interest, such as NSRF, a master neural developmental PLOS COMPUTATIONAL BIOLOGY regulator essential for gastrulation that may also influence the expression of thousands of genes during development [53][54][55][56] and OCT1, an essential regulator of development that plays crucial roles in the earliest cell fate decisions during embryonic development [57][58][59], that may warrant further investigation.…”