miRNA-26a blocks interleukin-2-mediated migration and proliferation of non-small cell lung cancer cells via vascular cell adhesion molecule-1.

Background: Literatures have confirmed role of inflammatory mediators like interleukin-2 (IL-2) in non-small cell lung cancer (NSCLC). microRNA-26a (miR-26a) is involved in variety of signaling pathways and functions as tumor suppressor and regulating the responsible genes at posttranscriptional level. The aim of study was to study the correlation of IL-2 and miR-26a in lung cancer (LC) cells.

Methods: For the study we selected 32 subjects reported for NSCLC and 20 with chronic obstructive pulmonary disease (COPD) as control in the present study. For analysis, H-460 and H-226 cell lines were selected and received treatment of varying dose of IL-2 to study the effect of IL-2 on expression of miR-26a and vascular cell adhesion molecule-1 (VCAM-1). miR-26a mimic and miR-26a inhibitor were transfected to study the effect on progression and migration of tumor cell as well as on levels of VCAM-1.

Results: We evidenced that, expression of miR-26a was suppressed, whereas levels of IL-2 and VCAM-1 were increased in NSCLC tissues. IL-2 down-regulated the levels of miR-26a but upregulated the levels of VCAM-1 in H-460 and H-226 cells. miR-26a modulated the expression level of VCAM-1 via binding the 3'-UTR region. We found that miR-26a attenuated the migration and proliferation of H-460 and H-226 cells. IL-2 modulated the levels of miR-26a via activating p65 but not STAT-3.

Conclusions: All together, the finding of our study show that miR-26a blocks IL-2 mediated proliferation and migration of NSCLC via targeting VCAM-1.