miR-143-3p overexpression

YTHDC1 facilitated the cytoplasmic transfer of has_circ_0061179 by directly binding to the modified m6A site. Our findings suggest that hsa_circ_0061179 acts as the sponge of miR-143-3p to activate TIMELESS signaling and inhibits DNA damage and apoptosis in OC cells.

LINC00667 is up-regulated in ccRCC and enhances the ZEB1 expression by targeting miR-143-3p, which in turn accelerates ccRCC progression and induces chemoresistance.

In summary, this is the first study to report that miR-143-3p overexpression in prostate cancer may inhibit EMT by targeting AKT1. The findings suggest miR-143-3p could be a useful diagnostic and prognostic biomarker for prostate cancer.

Hsa_circ_0084003, as a carcinogenic circular RNA, regulated its downstream target DNA methyltransferase 3A to promote pancreatic ductal adenocarcinoma cell aerobic glycolysis and epithelial-mesenchymal transition through sponging hsa-miR-143-3p. Therefore, hsa_circ_0084003 could be studied as a possible therapeutic target regarding pancreatic ductal adenocarcinoma.

In conclusion, the substitution of this miRNA during BEV treatment may help overcome BEV resistance, and this may be used as a novel treatment strategy in clinical settings. Implications: Continuous administration of VEGFA antibody upregulates SERPINE1/PAI1 expression via the downregulation of miR-143-3p, which contributes to acquiring bevacizumab resistance in ovarian cancer.

In conclusion, FNDC1 promotes the malignant prototypes of NSCLC cells. miR-143-3p is a negative regulator of FNDC1 in NSCLC cells, which may serve as a promising therapeutic target in NSCLC.

Meanwhile, overexpression of k-Ras reversed the inhibitory effects on WT cells induced by miR-143-3p mimics. Our findings indicate that miR-143-3p may be a potential novel prognostic biomarker and therapeutic target for WT.

We also discuss the potential role of miR-143-3p in FGFR signaling. Although this requires more extensive validation, it might be an interesting direction, since FGFR inhibition proved promising in preclinical studies in various cancers.

Knockdown of lncRNA AC008972.1 inhibits prostate cancer cell growth via downregulation of TAOK2 induced by miR-143-3p. LncRNA AC008972.1 acts as an oncogene in the progression of prostate cancer and may provide a novel therapeutic target for prostate cancer.

Exosomal miRNA transfer as a communication mode between PSCs and β-cells, which may be explored for its therapeutic utility.

LINC01426 accelerated the malignant progression of NSCLC. Mechanistically, LINC01426 acted as a competing endogenous RNA (ceRNA) for miR-143-3p to upregulate USP28 expression.

The present results suggest that silencing lncRNA SLC16A1-AS1 can induce ferroptosis through miR-143-3p/SLC7A11 signaling in renal cancer. Our study provided a novel view into the pathogenesis and treatment strategy of RCC.