MicroRNA-494 Modulation in Cancer Biology

MicroRNA-494 (miR-494) is a critical regulator of gene expression in a spectrum of human malignancies. By binding to complementary sequences in target mRNAs, miR-494 can act as either an oncogene or a tumour suppressor, depending on cellular context. Aberrant upregulation of miR-494 has been linked to enhanced cell proliferation, invasion and resistance to chemotherapy through the suppression of key tumour-suppressor genes such as PTEN and APC, and via activation of oncogenic pathways including PI3K/AKT and Wnt/β-catenin. Conversely, loss of miR-494 expression in certain cancer types relieves repression of pro-metastatic kinases, thereby enabling metastatic spread. miR-494 also influences endothelial and epithelial plasticity by modulating TGF-β/SMAD-mediated transitions, contributing to tumour angiogenesis and dissemination. The dualistic role of miR-494 across diverse tumour contexts underscores its global significance as both a biomarker for prognosis and a candidate for targeted therapeutic intervention.

Research from Nature Portfolio

Recent studies have elucidated mechanistic roles of miR-494 in solid tumours. In non-small cell lung cancer, elevated miR-494 promotes cell proliferation and confers cisplatin resistance by directly targeting caspase-2, thereby dampening apoptosis and enhancing colony formation. In hepatocellular carcinoma, miR-494 has been shown to induce an endothelial–mesenchymal transition by suppressing SIRT3 and activating the TGF-β/SMAD axis, facilitating tumour progression in vivo; antagonism of miR-494 in xenograft models mitigated metastatic growth. Another investigation in hepatocellular carcinoma identified miR-494-3p as a potent driver of PI3K/AKT pathway hyperactivation via PTEN repression, correlating with aggressive clinicopathological features and poor patient survival.

MicroRNA-494 Modulation in Cancer Biology publication trend

The graph below shows the total number of articles in microrna-494 modulation in cancer biology across all publications each year (not limited to Nature Index journals).

Technical terms

MicroRNA (miRNA): short non-coding RNA molecules that regulate gene expression post-transcriptionally.

OncomiR: microRNA with oncogenic functions that promote tumour development and progression.

Tumour-suppressor miRNA: microRNA that inhibits cancer cell growth or metastasis by targeting oncogenes.

Endothelial–mesenchymal transition (EndMT): process by which endothelial cells acquire mesenchymal traits, facilitating metastasis.

PI3K/AKT signalling pathway: intracellular cascade that regulates cell growth, survival and metabolism, often hyperactivated in cancer.

TGF-β/SMAD pathway: signalling axis where transforming growth factor-β activates SMAD transcription factors to regulate cell differentiation and migration.

References

1. MicroRNA-494 promotes cancer progression and targets adenomatous polyposis coli in colorectal cancer. Molecular Cancer (2018).
2. MiR-494 acts as a tumor promoter by targeting CASP2 in non-small cell lung cancer. Scientific Reports (2019).
3. miR-494 induces EndMT and promotes the development of HCC (Hepatocellular Carcinoma) by targeting SIRT3/TGF-β/SMAD signaling pathway. Scientific Reports (2019).
4. MiR-494-3p promotes PI3K/AKT pathway hyperactivation and human hepatocellular carcinoma progression by targeting PTEN. Scientific Reports (2018).
5. The epigenetically regulated miR-494 associates with stem-cell phenotype and induces sorafenib resistance in hepatocellular carcinoma. Cell Death & Disease (2018).
6. MicroRNA-494 inhibits breast cancer progression by directly targeting PAK1. Cell Death & Disease (2017).