MIR638 (MicroRNA 638)

Priorities for validation include reporter assays, gene/protein modulation, phenotypic rescue, and in vivo testing in MP-exposed models. Collectively, our results nominate miRNAs as candidate tools to interrogate and potentially mitigate MP-associated carcinogenic mechanisms.

PART1 negatively regulated miR-638 expression, and inhibition of miR-638 reduced the protective effect of the knockdown of PART1 on OGD/R-treated cells. This study demonstrated that knockdown of PART1 inhibits IS-induced neurological injury by regulating miR-638 expression, which promotes the understanding of IS disease and provides new options for the treatment of the disease.

THP-1 and HL-60 cells stably overexpressing circTADA2A exhibited reduced cell proliferation, and sensitized cell to ferroptosis by a ferroptosis inducer RSL3...Mechanistically, circTADA2A act as a sponge for miR-638, and upregulation of miR-638 expression could restore cellular phenotypes induced by circTADA2A. Our findings demonstrated that circTADA2A suppresses cell proliferation and promotes ferroptosis by sponging miR-638 during AML progression.

Extracellular vesicle miRNAs add a layer of complexity, acting as mediators in CD's systemic effects. Finally, we outline future perspectives, envisioning how the evolving landscape of miRNA research can propel advancements in understanding, diagnosis, and treatment, marking this review as a cornerstone for researchers and clinicians in the dynamic field of miRNAs and CD.

Our findings suggest that differentiation of cell subpopulations is regulated by specific miRNAs. Furthermore, miRNA-based strategies may be developed for immunotherapeutic treatments of AML.

 Our results indicated that circSXN27 facilitated GC progression by acting as a sponge of miR-638.

The study findings encourage us to hypothesize that the aforementioned miRNAs may contribute to the predominance of aGVHD, particularly low-grade cutaneous aGVHD.

Mimic miR-638-5p transfection inhibited MDA-MB-231 cell proliferation and reduced migration and expression of CFL1, SIX4, and MAZ genes was decreased in mimic miR-638-5p transfected cells. These findings suggest that curcumin exerts its anticancer effects on MDA-MB-231 cells by modulating the expression of miR-638-5p and its possible target genes.

Furthermore, four putative target genes of these two miRNAs were identified (ADH1B, CTH, FTCD, RCL1), which were significantly associated with TACE response, immune score, immunosuppressive immune cells infiltration, PDCD1 and CTLA4. The HCC-HRMs signature may be utilized as a promising prognostic factor and may have implications for guiding TACE and immune therapy.

We highlighted that miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under tetrandrine treatment.

Distinct miRNA expression profiles are associated with clinical outcomes of low-grade CIN. The functional effects of the differentially expressed miRNAs may be biological determinants of CIN progression or resolution.

Our results demonstrated that circNCOR1 bounds to hsa-miR-638 and targets CDK2, thereby regulating the radiosensitivity of TNBC.