MIR34B (MicroRNA 34b)

ML enables multidimensional analysis of EGT transfer curves and extraction of physically meaningful features from high-dimensional data. This approach advances point-of-care technologies for highly sensitive and selective miRNA detection, with strong potential for portable molecular diagnostics.

Pathway enrichment analyses indicated that the target genes of dysregulated miRNAs were enriched in cancer-related pathways and processes involving nucleic acid metabolism. Given the reported increased cancer risk among azoospermic patients, these findings suggest that specific miRNAs in seminal plasma may serve as novel non-invasive biomarkers and point to shared molecular mechanisms potentially linking NOA and cancer etiology.

Indeed, for the pairs miR-127-5p/miR-125b-5p, miR-148a-3p/miR-125b-5p, miR-148a-3p/miR-132-3p, and miR-34b-3p/miR-193a-5p, common mRNA targets and involvement in biological processes, including pathways associated with epigenetic regulation, proliferation, and metastasis, were revealed. The miRNA-mRNA regulatory network constructed involving DNMTs and EZH2 highlights their potential role in breast cancer progression and demonstrates diagnostic and prognostic significance.

Downregulated miR-34b-3p expression promoted OSCC progression by enhancing cellular activities and upregulating the expression of pro-angiogenic factors via targeting SOX5.

Clinically, HER3 and PHF8 expression levels were positively correlated in TNBC tissue specimens, and TCGA dataset analyses indicated that the HER3/miR-34b-5p/PHF8 axis is significantly associated with poor survival outcomes in breast cancer patients. Collectively, our findings establish a novel epigenetic regulatory circuit through which HER3 drives TNBC progression and lay the groundwork for future therapeutic strategies aimed at disrupting HER3-epigenetic crosstalk in TNBC.

In contrast, SNHG4 knockdown aggravated FFA-induced lipid metabolic and inflammatory disorders, whilst this effect was rescued by inhibiting miR-34b-5p. SNHG4 regulates lipid metabolism and inflammatory disorders in NAFLD by targeting the miR-34b-5p/XIAP axis.

In summary, we discovered that ablation of miR-34/449 led to hyperactivation of the Wnt/β-catenin signaling pathway, which resulted in the differentiation impairment of ciliated cells, thus resulting in infertility in the mice. This study revealed a novel mechanism describing how miR-34/449 affects oviductal ciliated cell differentiation and oviductal epithelial homeostasis through the Wnt/β-catenin signaling pathway and finally affects fertility.

The expression levels of miR-34b, TP53, and BRD4 genes, along with the migration rates and sensitivity to the BRD4-specific inhibitor JQ1, were compared between the miR-34b overexpressing cells...This finding aligns with prior reports indicating a negative correlation between miR-34b levels and survival rates in patients with TNBC. These insights may provide new perspectives on the role of miR-34b in the development and progression of TNBC.

A novel, non-invasive, liquid biopsy-based method for patients with EGC may predict those conventionally classified as high-risk patients with LNM who are unlikely to benefit from surgical resection.

BAs facilitate GIM partially via a PVT1/miR-34b-5p/HNF4α positive feedback loop. PVT1 may become a novel target for blocking the continuous development of GIM and preventing the initiation of gastric cancer in patients with bile reflux.

This study provides evidence for the association between the miR-34b/c rs4938723 polymorphism and hepatoblastoma risk in Chinese Han children from East China, suggesting that this polymorphism may have potential as a biomarker for predicting hepatoblastoma susceptibility in this specific population.

microRNAs selected in this work can regulate gene expression trough 3'UTR region of EMT-transcription factors. In BC cells, miR-196a-5p and miR-22-3p decrease ZEB1 levels, being novel modulators of EMT. Also, the eight evaluated microRNAs, reduced the metastatic hallmarks in BC cells.