MicroRNA-182 Roles in Cancer Biology

MicroRNA-182 (miR-182) is a small non-coding RNA that exerts critical control over gene expression by binding to messenger RNAs, leading to translational repression or degradation. In diverse malignancies, miR-182 levels are frequently dysregulated, acting either as an oncomiR that promotes proliferation, invasion, metastasis and chemoresistance or as a tumour suppressor that induces cell cycle arrest and apoptosis. Its dual-role nature reflects the context-dependent targeting of key regulators in pathways such as JAK/STAT3, Wnt/β-catenin, TGF-β, PI3K/Akt and hypoxia-inducible factor signalling. Aberrant miR-182 expression has been linked to epithelial-to-mesenchymal transition, angiogenesis, immune evasion and response to therapy. Across solid tumours and haematological malignancies, miR-182 continues to emerge as both a candidate biomarker for diagnosis and prognosis and as a potential node for therapeutic intervention.

Research from Nature Portfolio

Studies have elucidated how hypoxia-responsive miR-182 sustains activation of hypoxia-inducible factor 1α by directly targeting its negative regulators, prolyl hydroxylase domain 2 and FIH1. Overexpression of miR-182 in prostate cancer cells elevates HIF1α under normoxic and hypoxic conditions, enhances angiogenic capacity in in vitro assays and accelerates tumour growth in animal models. Conversely, inhibition of miR-182 restores these regulators, diminishing HIF1α levels and vessel formation. These findings reveal a feed-forward loop that enables malignant cells to adapt to low-oxygen microenvironments and promote vascular expansion.

MicroRNA-182 Roles in Cancer Biology publication trend

The graph below shows the total number of articles in microrna-182 roles in cancer biology across all publications each year (not limited to Nature Index journals).

Technical terms

microRNA: A short non-coding RNA molecule that regulates gene expression by pairing with target mRNAs, leading to their degradation or translational inhibition.

OncomiR: A microRNA whose upregulation contributes to tumorigenesis by downregulating tumour suppressor genes.

Tumour suppressor microRNA: A microRNA that prevents tumour development by inhibiting oncogenes or pro-survival factors.

Epithelial-to-mesenchymal transition (EMT): A biological process in which epithelial cells acquire mesenchymal traits, enhancing motility and invasiveness.

DNA hypermethylation: The addition of methyl groups to cytosine residues in gene promoter regions, often resulting in transcriptional silencing.

Hypoxia-inducible factor 1α (HIF1α): A transcription factor stabilised under low oxygen conditions that drives the expression of genes involved in angiogenesis and metabolic adaptation.

Angiogenesis: The formation of new blood vessels from pre-existing vasculature, essential for tumour growth and metastasis.

References

1. The emerging role of MicroRNA-182 in tumorigenesis; a promising therapeutic target. Cancer Cell International (2023).
2. Hypoxia-inducible miR-182 enhances HIF1α signaling via targeting PHD2 and FIH1 in prostate cancer. Scientific Reports (2015).
3. Low expression of miR-182 caused by DNA hypermethylation accelerates acute lymphocyte leukemia development by targeting PBX3 and BCL2: miR-182 promoter methylation is a predictive marker for hypomethylation agents + BCL2 inhibitor venetoclax. Clinical Epigenetics (2024).
4. MiR-182 Is Upregulated in Prostate Cancer and Contributes to Tumor Progression by Targeting MITF. International Journal of Molecular Sciences (2023).