miR-23a expression

The connection between miRNA expression changes, the increase in glutathione-S-transferase and especially the decrease in superoxide dismutase activities in patients with white lesion potential malignant transformation using the provided statistical analysis was confirmed.

miR-23a targeted HOXC8, which reversed miR-23a-mediated cell viability and migration. HPV16 E7-mediated miR-23a suppressed CC cell viability and migration by targeting HOXC8, suggesting a novel mechanism of HPV-induced CC.

In conclusion, Exo miR-23a-5p inhibited HCC proliferation and angiogenesis by regulating PRDX2 expression. Our results revealed the role and specific molecular mechanism of exo miR-23a-5p in regulating HCC progression.

miR-23a can significantly alleviate sepsis-induced lung injury in CLP-induced septic mice and LPS-stimulated cell lines by suppressing NLRP3 inflammasome activation and inflammatory response, while promoting the CXCR4/PTEN/PI3K/AKT pathway.

the antitumor effects of JHD on HCC are mediated at least in part by inhibition of EMT due to downregulation of exosome-mediated intercellular miR-23a-3p transfer and subsequent blockade of Smad signaling. Disrupting this exosomal miR-23a-3p/Smad signaling pathway may be an effective treatment.

Together, these findings strongly suggest that miR-23a acts as a tumor suppressor by downregulating CRYAB expression. Restoration of miR-23a by chidamide may therefore have a therapeutic effect in controlling the sensitivity of CML cells to imatinib.

Overexpression of Runx2 reverses the tumor-suppressive effect of miR-23a-3p. miR-23a-3p can inhibit the PI3K/Akt signaling pathway by targeting Runx2 and inhibit the malignant evolution of oral cancer.

ZNF674-AS1 inhibits the migration and invasion of NSCLC cells by regulating a miR-23a/E-cadherin axis. ZNF674-AS1 and miR-23a could become potential therapeutic targets for NSCLC.

Resveratrol ameliorated glucose uptake and lipid metabolism of the GDM mice and adipocytes with IR by regulating miR-23a-3p/NOV axis.

miR-451a expression was associated with ER, HER-2 status and anthracyclines. A miRNA signature of chemotherapeutic response may be clinically valuable for improving current chemotherapy regimens of individual treatment for patients with breast cancer.

In summary, our findings report a new molecular mechanism for the miR-27a-3p-mediated Taxol resistance via targeting tumour suppressor, Fbxw7 in osteosarcoma. This study potentiates a miRNA-based therapeutic approach against Taxol resistant osteosarcoma.

The myeloperoxidase (MPO) activity and the expression of interleukin 6 (IL-6), IL-1β, IL-10, and tumor necrosis factor-α (TNF-α) were detected. High expression of the lncRNA MALAT1 and MCEMP1, as well as low expression of miR-23a, was observed in septic mice. LncRNA MALAT1 competitively bound to miR-23a, and miR-23a targeted MCEMP1. Moreover, the down-regulation of lncRNA MALAT1 repressed the expression of MPO, IL-6, IL-10, TNF-α, and IL-1β. Silencing of lncRNA MALAT1 or overexpression of miR-23a reduced inflammation, inhibited cell proliferation, and promoted cell apoptosis in septic mice. Taken together, MALAT1 promotes the inflammation in septic mice by binding to miR-23a to up-regulate MCEMP1. Therefore, silencing of lncRNA MALAT1 might provide a novel therapeutic target for sepsis.