miR-200-c overexpression

This work determines the mechanisms by which MET in CAFs via miR-200c transcriptional enrichment with DNA demethylation triggered by oxidative stress promotes cancer progression. CAFs undergoing MET trans-differentiation and senescence coordinate heterotypic signaling that may be targeted as an anti-cancer strategy.

In addition, a local administration of pDNA miR-200c using CaCO delivery significantly enhanced miR-200c transfection and suppressed tumor growth of CDX in mice. These results strongly indicate that the nanocomplexes of CaCO/pDNA miR-200c may potentially be used to reduce oral cancer recurrence and improve clinical outcomes in OSCC treatment, while more comprehensive examinations to confirm the safety and efficacy of the CaCO/pDNA miR-200c system using various preclinical models are needed.

In conclusion, patients with high miR-200c expression GC had better survival despite association with aggressive tumor biology, such as high mutation rates, cell proliferation, and low cancer immunity. Given that low miR-200c GC was associated with hypoxia, angiogenesis, EMT and TGF-β signaling, we cannot help but speculate that the difference in survival by miR-200c expression may be at least partly due to the association between low miR-200c expression and aggressive biology.

We showed that ALDH was upregulated upon ZEB1-suppressed miRNA transfection (Mann-Whitney ** p = 0.009, t-test ** p = 0.009, t-test ** p = 0.002, and t-test *** p = 0.0006). Overall, our study enabled an improved understanding of the role of ZEB1-suppressed miRNAs in CSC biology.

Besides upregulating the ICs, this had substantial cellular consequences including an induction of interferon type I and type III expression, increased levels of intracellular dsRNA sensors, and a significantly altered cellular growth and apoptotic activity.Our study highlights the capability of miRNA mimics to non-specifically induce a dsRNA-mediated antiviral interferon response. Consequently, phenotypic alterations crucially distort physiological miRNA functions and might result in a major misinterpretation of previous and future miRNA studies, especially in the context of IC regulation.