Over-expression of miR126 in a lung cancer cell line resulted in a decrease in Crk protein without any alteration in the associated mRNA.

inhibits growth of lung cancer cells

miR-126 can inhibit proliferation of non-small cell lung cancer cells through one of its targets, EGFL7.

let-7b and miR-126 are down-regulated in tumor tissue and correlate with microvessel density and survival outcomes in non--small--cell lung cancer.

miR-126 downregulation is associated with lung metastasis in breast cancer.

Our results suggest that miR-126 might play tumor-suppressive and miR-200c an oncogenic role in non-small cell lung cancer

These findings suggested that miR-126 and miR-133b might play a key role in the progression and metastasis of non small cell lung cancer

miR-126 was slightly expressed in non-small-cell lung cancer (NSCLC) A549 cells and was negatively associated with the expression of PIK3R2; upregulation of miR-126 in NSCLC A549 cells can reduce the expression of the target gene PIK3R2 and influence the PTEN/PI3K/AKT signaling pathway, suppressing the proliferation, migration, and invasive abilities of A549 cells

MiR-126-3p and miR-451a predicted the severity of lung adenocarcinoma.

exosome-enriched miR-126 from normal endothelial cells inhibited cell growth and induces loss of malignancy of non-small cell lung cancer cells. These findings suggest a role of exo-miRs in the modulation of the NSCLC microenvironmental niche.

Thus, our results indicated that lncRNA-PVT1-5 may function as a competing endogenous RNA (ceRNA) for miR-126 to promote cell proliferation by regulating the miR-126/SLC7A5 pathway, suggesting that lncRNA-PVT1-5 plays a crucial role in lung cancer progression and lncRNA-PVT1-5/miR-126/SLC7A5 regulatory network may shed light on tumorigenesis in lung cancer.

expression of miR-126-5p suppresses the enzymatic activity of MDH1, mitochondrial respiration and caused cell death in non-small cell lung carcinoma cell lines.

miR-126 levels were significantly higher in the bronchoalveolar lavage fluid of lung adenocarcinoma patients than in control subjects. lung adenocarcinoma tissues showed increased expression of miR-126 compared to normal tissue samples.

Dysfunction of MINCR, miR-126 and SLC7A5 predicted poor prognosis of patients with non-small cell lung cancer.

Study results indicated that the coregulation of miRNA1263p and miRNA1265p plays a key role in the development of lung adenocarcinoma, which also suggests a failproof mode between miRNA1263p and miRNA1265p.

MiR-126-3p was significantly down-regulated in non-small cell lung cancer (NSCLC) cell lines and tissues. The up-regulation of miR-126-3p inhibited the growth, colony formation, migration and invasion of NSCLC cell. Xenograft model indicated that miR-126-3p suppressed NSCLC cell growth and lung metastasis by targeting chemokine (C-C motif) receptor 1 (CCR1).

The expression level of miR-126-5p is lowered in lung adenocarcinoma tissue, and patients with lung adenocarcinoma have lower serum level of miR-126-5p than healthy subjects. A high expression of miR-126-5p is associated with a more favorable prognosis of the patients than a low expression.

Long non-coding RNA PRNCR1 modulates non-small cell lung cancer cell proliferation, apoptosis, migration, invasion, and EMT through PRNCR1/miR-126-5p/MTDH axis.

Circulating miR-21-5p and miR-126-3p: diagnostic, prognostic value, and multivariate analysis in non-small-cell lung cancer.