MIR198 (MicroRNA 198)

[This retracts the article DOI: 10.3727/096504017X14944585873631.].

Importantly, overexpression of MYD88 mitigated the inhibitory effect exerted by miR-198-5p-rich IR-EVs on M2 polarization of macrophages. Our findings indicate that EVs rich in miR-198-5p derived from irradiated OSCC cells inhibit M2 polarization of macrophages through inhibition of MYD88 expression; thus suggesting that encapsulating miR-198-5p within EVs may represent a promising therapeutic strategy for OSCC.

Our findings demonstrate that angiomiR expression patterns are impacted by isolation methods. Instead of relying on ECs cultured in vitro , we suggest careful validation studies of cells freshly collected from tumors before determining whether a miRNA is a bona fide angiomiR.

Our study uncovered the central role of Dicer in the M2 polarization of TAMs, in turn suggesting a promising therapeutic strategy for CRLM.

These findings both reinforce our current understanding of prostate cancer's molecular landscape and point to unexplored pathways that could lead to novel therapeutic strategies. By mapping these regulatory relationships, our work contributes to the growing knowledge base needed for developing more targeted and effective treatments.

We have found miR-198 to be upregulated in OSCC cells treated with 5-Azacytidine, a known DNA methyltransferase inhibitor...Delivery of a synthetic miR-198 mimic to OSCC cells results in a significant decrease in xenograft size in nude mice, potentiating its use in therapeutics. These results suggest that miR-198 is epigenetically silenced in OSCC, which promotes tumor growth, in part, by upregulating the levels of TOPORS.

The hsa_circ_0009910/miRNA-198/c-Met interaction network affects the viability, but not apoptosis, of HeLa cells. Based on this mechanism, the present study suggests that hsa_circ_0009910 may be a promising biomarker for CC.

However, challenges persist in developing safe and efficient delivery strategies to target miRNAs specifically, minimizing off-target effects and enhancing therapeutic outcomes. Future mechanistic pre-clinical and clinical research would contribute to overcoming these challenges.

Moreover, we used LGA-PEI (LPNP) nanoparticles to effectively administer miR-198 to tumors in vivo, inducing tumor sensitization to gemcitabine and leading to a significant reduction in tumor burden and metastases and a concomitant downregulation of VCP expression and autophagy maturation. Our results indicate a potential therapeutic strategy for targeting gemcitabine resistant PDAC and establishes the use of LPNPs for effective therapeutic delivery of nucleic acids in vitro and in vivo.

Our study revealed the dysfunctional transport of nutrients and trace elements may be common pathogenesis of pancreatic ductal adenocarcinoma and chronic pancreatitis. Examination on these common pathways and real hub genes may shed light on the underlying mechanism.

And the absence of circMFN2 inhibited tumor growth in vivo. CircMFN2 repressed OC progression by regulating the miR-198/CUL4B axis.