miR‐223 overexpression

Our study demonstrated that circ_0124346 regulates lipid metabolism in PAAD cells via the miR-223-3p/ACSL3 axis, suggesting that targeting circ_0124346 may serve as a potential strategy for treating PAAD and assisting in its diagnosis.

miR-223-3p inhibits the migration of OSCC cells, while miR-155-5p can elevate the miR-223-3p mRNA expression. The simultaneous miR-155-5p overexpression and miR-223-3p inhibition can activate pEMT, increasing OSCC migration in vitro. This provides a novel approach and potential target for the effective treatment of OSCC.

In the AGA cell model, lncRNA SNHG14, as an miR-223-3p sponge, induces a cellular inflammatory response by controlling the level of miR-223-3p, so aggravating the disease progress of AGA.

Our data suggest a potential role for miR-233-3p as a prognostic as well as a therapeutic target for HCC.

Lastly, miR-223-3p inhibited ONG growth. miR-223-3p plays an inhibitory role in ONG development by regulating NLRP3 to inhibit the proliferation of ONG cells and promote apoptosis.

Finally, to explore the therapeutic potential of miR-233 in liver fibrosis, we generated co-cultured organoids of HSCs with Huh7 hepatoma cells and challenged them with acetaminophen (APAP) or palmitic acid (PA) to induce hepatotoxicity. We showed that ectopic expression of miR-223 in HSCs attenuated fibrogenesis in the two human organoid models of liver injury, suggesting its potential application in antifibrotic therapy.

MiR-21 was over-expressed in patients with gastric precancerous conditions irrespective of etiology, while in the same subgroups miR-142 and miR-223 were under-expressed compared to healthy controls. Controlling miRNAs up- or downregulation could lead to a breakthrough in treating chronic autoimmune diseases and potentially interfere with the progression to cancer.

The animal test revealed that compared with the mimic-NC+ oe-NC group, miR-223-3p mimic+ oe-NC group showed reduced tumor volume and decreased Ki67 expression (both P<0.05); while compared with miR-223-3p mimic+ oe-NC group, miR-223-3p mimic+ oe-NLRP3 group had increased tumor volume and increased Ki67 expression (both P<0.05). It was concluded that overexpression of miR-223-3p can effectively inhibit the expression of NLRP3 and cell pyroptosis in MDS.

It is the first time we investigated the potential role and ceRNA regulatory mechanism of PITPNA-AS1 in LUSC. The data disclosed that PITPNA-AS1 upregulated PTN through sponging miR-223-3p to enhance the onset and progression of LUSC. These findings suggested the ceRNA axis may serve as a promising therapeutic biomarker for LUSC patients.

The xenograft experiments in nude mice also proved the antitumor effect of circLRCH3. These results suggested that the circLRCH3/miR-223/LPP axis likely plays a critical role in CRC.

FGD5-AS1 directly sponged miR-223 and promoted the expression of ECT2 and FAT1 in HCC, thus enhancing HCC cell proliferation and stemness. Our study identifies potential prognostic biomarkers and therapeutic targets for HCC.