MicroRNA-186 Modulation in Cancer Progression

MicroRNA-186 (miR-186) is a short non-coding RNA that regulates gene expression post-transcriptionally and exerts context-dependent roles across a spectrum of human malignancies. In many solid tumours miR-186 acts as a tumour suppressor, limiting proliferation, invasion, migration and angiogenesis through direct targeting of oncogenic transcripts. Conversely, in certain contexts it may enhance malignant traits by repressing tumour-suppressive networks. Mechanistically, miR-186 influences key signalling cascades, including AKT-GSK3β-β-catenin, HIF-1α-driven hypoxic responses and epithelial–mesenchymal transition programmes. By modulating the stability or translation of mRNAs encoding factors such as kinesin family member 2C, protein kinase Cα, Twist1 and ABCB1, miR-186 shapes tumour metabolism, vascular remodelling, immune evasion and sensitivity to chemotherapeutics. Preclinical models demonstrate that restoring or inhibiting miR-186 can alter xenograft growth, metastasis and drug response, highlighting its potential as both a biomarker and a therapeutic target. Ongoing efforts aim to harness miR-186 modulation for precision oncology, with implications for diverse cancers including lung, gastric, ovarian and prostate.

Research from Nature Portfolio

Recent studies in non-small cell lung carcinoma have revealed that miR-186-3p directly binds to the 3′-untranslated region of kinesin family member 2C, suppressing its expression and thereby attenuating AKT-GSK3β-β-catenin signalling. Ectopic elevation of miR-186-3p in lung cancer cell lines reduces proliferation, migration and invasion while promoting apoptosis. Conversely, downregulation of miR-186-3p correlates with poor prognosis, underscoring its tumour-suppressive role and therapeutic promise in lung malignancies.

MicroRNA-186 Modulation in Cancer Progression publication trend

The graph below shows the total number of articles in microrna-186 modulation in cancer progression across all publications each year (not limited to Nature Index journals).

Technical terms

MicroRNA: Short RNA molecule (~22 nucleotides) that binds target mRNAs to inhibit translation or induce degradation.

Angiogenesis: Formation of new blood vessels from existing vasculature, critical for tumour growth and dissemination.

Epithelial–mesenchymal transition (EMT): Cellular programme conferring migratory and invasive properties by shifting epithelial cells toward a mesenchymal phenotype.

Glycolysis: Metabolic pathway converting glucose to lactate, often upregulated in cancer cells even under aerobic conditions.

3′-Untranslated region (3′-UTR): Segment of mRNA downstream of the coding sequence that contains regulatory elements for post-transcriptional control.

Xenograft: Tumour model generated by implanting human cancer cells into immunocompromised animals to study in vivo behaviour.

References

1. KIF2C accelerates the development of non-small cell lung cancer and is suppressed by miR-186-3p via the AKT-GSK3β-β-catenin pathway. Scientific Reports (2023).
2. Hypoxia-induced downregulation of microRNA-186-5p in endothelial cells promotes non-small cell lung cancer angiogenesis by upregulating protein kinase C alpha. Molecular Therapy - Nucleic Acids (2023).
3. MiR-186 inhibited aerobic glycolysis in gastric cancer via HIF-1α regulation. Oncogenesis (2016).
4. MicroRNA-186 induces sensitivity of ovarian cancer cells to paclitaxel and cisplatin by targeting ABCB1. Journal of Ovarian Research (2015).
5. miR-186 affects the proliferation, invasion and migration of human gastric cancer by inhibition of Twist1. Oncotarget (2016).