High levels of MIR16 is associated with non-small-cell lung cancer.

These findings clearly suggest that the downregulation of miR-15a-16 with Cripto amplification may be involved in the development of nonsmall cell lung cancer.

The miR-16 directly targeted anti-apoptotic protein Bcl-2 in paclitaxel resistant lung cancer cells

Results showed that miR-16-1 overexpression significantly inhibited cell proliferation and induced apoptosis in lung cancer when compared with the control group.

Data indicate that miR-9, miR-16, miR-205 and miR-486 may serve as non-small cell lung cancer (NSCLC) biomarkers.

Results revealed that miR-16 was significantly downregulated, and ATG3 was significantly upregulated in non-small cell lung carcinoma (NSCLC) patient tissue samples. ATG3 was found to be a direct target of miR-16. Finally, the study showed that miR-16 overexpression rescued TGF-beta1mediated inhibition of autophagy and plays important roles in the EMT of NSCLC cells.

MicroRNA-16 inhibits the proliferation, migration and invasion of non-small cell lung carcinoma cells by down-regulating matrix metalloproteinase-19 expression.

Decreased miR-16 expression may play a role in upregulating expression of MEK1 and promoting proliferation and invasion of lung cancer cells.

Circ0021205 aggravates the progression of non-small cell lung cancer by targeting miRNA-16-5p/VEGFA.

Integrative data modeling from lung and lymphatic cancer predicts functional roles for miR-34a and miR-16 in cell fate regulation.

Long noncoding RNA Linc00210 promotes non-small cell lung cancer progression via sponging miR-16-5p/PTK2 axis.