miR-26a expression inhibited the expression of enhancer of zeste homolog 2 and transactivated downstream target genes, which suggests that EZH2 is a potential target of miR-26a; miR-26a plays an important role as an anti-oncogene in the molecular mechanism of lung cancer

Our study demonstrated that miR-26a enhanced lung cancer cell metastasis potential via modulation of metastasis-related gene expression, and activation of AKT pathway by PTEN suppression

miR-26a is involved in the TLR9mediated growth and migration of lung cancer through the PI3K-Akt signaling pathway.

Reduced miR26a expression is associated with non-small cell lung cancer in comparison to chronic obstructive pulmonary diseases.

we found that miR-26a confers epidermal growth factor receptor-targeted tyrosine kinase inhibitors resistance of non-small cell lung cancer cells by targeting and silencing PTPN13

The results of our pilot study indicated the diagnostic potential of miR-29b and MMP-2, an inverse association between miR-26a and MMP-2, and proved the role of MMP-2 and miR-26a, miR-29b and miR-519d in lung carcinogenesis

Further analyses indicated that KHSRP was involved in miR-26a maturation and inhibited the expression of PTEN in small cell lung cancer cells

The overexpression of miR26a in a lung adenocarcinoma cell line repressed cell migration, invasion and growth by targeting high mobility group A1.

Overexpression of miR-26a in docetaxel-resistant advanced lung adenocarcinoma cells could decrease the proliferation, increase the apoptosis rate and reverse EMT to MET of docetaxel-resistant advanced lung adenocarcinoma cells both in vivo and vitro and such function is partially exerted via downregulating EZH2.

miR-26a enhances migration and invasion of lung cancer cells in vivo and in vitro. GSK3beta is a direct target of miR-26a.

MiR-26a functions as a tumor suppressor in ambient particulate matter-bound metal-triggered lung cancer.LIN28B was a direct target of miR-26a.

miR-26a-5p enhances lung cancer cell metastasis via activation of JAK2/STAT3 pathway.

Data suggested that ANXA1 negatively regulated miR-26a expression in non-small cell lung cancer (NSCLC). In the other hand, miR-26a negatively regulated NF-kappaB activation in NSCLC.