miR-31 acts as an oncogenic miRNA (oncomir) in lung cancer by targeting specific tumor suppressors for repression.

Knock-down of C/EBP-beta abrogated CSC-mediated activation of LOC554202. Over-expression of miR-31 significantly enhanced proliferation and tumorigenicity of lung cancer cells; knock-down of miR-31 inhibited growth of these cells

findings indicate that reduced miR-31 and let-7 are involved in maintaining the balance between differentiation and quiescence in lung cancer stem-like side population cells

Upregulation of miR-31-5p is associated with non-small cell lung cancer.

MicroRNA-31 predicts the presence of lymph node metastases and survival in patients with lung adenocarcinoma.

These results demonstrated that miR- 31-targets interactions play a central role in the regulation of lung cancer-related genes and their pathways as well as network

miR-31 may play a pleiotropic role in the development of lung cancers among different histological types.

Results suggest that miR-31 may be a suppressor that regulates an essential oncogenic pathway, the loss of which may promote lung carcinogenesis.

miRNA-31 may be a molecular marker for the diagnostic and prognostic evaluation of primary lung cancer.

results suggest that miR-31 might inhibit the growth of lung adenocarcinoma cancer stem-like cells via down regulation of the MET-PI3K-Akt signaling pathway

High miR31 expression is associated with lung cancer progression.

Reduction of miR-31 expression enhanced lung cancer proliferation and migration by repressing HuR expression

Using a combination of cytokine expression profiling and miRNAs algorithms, we identified VEGFA/CCL2 and FOXO3a as direct targets of miR-1, miR-206 and miR-31, respectively. Importantly, systemic delivery of anti-VEGFA/CCL2 or pre-miR-1, pre-miR-206 and anti-miR-31 significantly inhibited tumor angiogenesis, TAMs accumulation, tumor growth and lung metastasis.

High miR31 expression is associated with lung cancer.