MIR330 (MicroRNA 330)

miR-330-5p was shown to affect the proliferation, invasion, and migration of gastric cancer cells by mediating ITGA5 through a mechanism possibly associated with the regulation of the FAK/AKT signaling pathway.

Also, METTL3 promoted the expression of circ_0003998 by m6A modification. METTL3-modified circ_0003998 promoted NSCLC cell malignancy through miR-330-5p/CXCL3 axis, suggesting that circ_0003998 might be a new treatment strategy for NSCLC.

Mast cell-derived exosomes, particularly those from activated cells (AE), exacerbated ECM neuronal injury through partial activation of ER stress pathways.

[This retracts the article DOI: 10.3389/fcell.2020.00827.].

Thus, significant metabolomic imbalance in the urine was observed in the OC patients and was associated with changes in the levels of microRNAs that regulate the signaling pathways of the metabolites. The 26 compounds with abnormal concentrations and the levels of the microRNAs miR-33b-5p, miR-423-5p, miR-6843-3p, miR-4668-3p, miR-30c-5p, miR-6743-5p, miR-4742-5p, miR-1207-5p, and miR-17-5p in the urine were considered to be suitable as noninvasive diagnostic markers of OC.

RT - qPCR validation confirmed significant expression differences of CD8A, ADAMDEC1, CD69, CRIP1, and BCL11B between SKCM and control samples. This study presents a robust prognostic model for SKCM based on PANoptosis - related genes, providing a theoretical foundation for SKCM treatment.

The circ-NOLC1 inhibits CC development through regulating the miR-330-5p-PALM signaling axis. This finding reveals a novel mechanism and identifies potential therapeutic targets, emphasizing the necessity for further regulatory studies and clinical validation.

miR-330-3p is a potential biomarker for PPUI and regulates the function of urethral fibroblasts by targeting MMP2.

Accordingly, the article is retracted as the editors consider its conclusions to be invalid. The authors have been informed of the decision of retraction but not available for a final confirmation.

Overexpressing VDAC1 or inhibiting miR-330-5p blocked the roles of silencing hsa_circ_0007905 on CSCs. Thus, we revealed the mechanism by which hsa_circ_0007905 competitively adsorbs miR-330-5p to mediate VDAC1 expression to promote stemness and inhibit apoptosis of CSCs in CC, offering an therapeutic target for treating CC.