Conclusions
MiR-507 was noticeably downregulated in NSCLC and correlated with poor prognosis of NSCLC patients. MiR-507 represses the invasion and proliferation of NSCLC via targeting ZEB2. This study indicated that miR-507 might serve as a potential therapeutic target for NSCLC.
Methods
Quantitative real-time PCR (qRT-PCR) assay was applied for the detection of miR-507 in NSCLC tissues and cell lines. Cell Counting Kit-8 (CCK-8) and colony formation assays were carried out to assess the proliferative abilities of NSCLC cells. Cell invasive capabilities were determined by transwell assays. We used Dual-Luciferase reporter assays to verify the binding between miR-507 and zinc finger E-box binding homeobox 2 (ZEB2).
Objective
Non-small cell lung cancer (NSCLC) is one of the most common malignancies around the world and effective therapeutic method is yet to be excavated for advance NSCLC. MicroRNA-507 (miR-507) was found to be aberrantly expressed and affected cancer cell behaviors in some types of cancers. However, the role of miR-507 in NSCLC is largely unknown. The expression, biological role, and the underlying mechanism of miR-507 in NSCLC were explored in this study. Patients and
Results
MiR-507 was found to be downregulated in NSCLC tissues and cell lines. Low expression of miR-507 was correlated with poor prognosis of NSCLC. Overexpression of miR-507 repressed NSCLC cell invasion and proliferation. ZEB2 was predicted to be a direct downstream molecular of miR-507 and their direct binding was verified by Dual-Luciferase reporter assays. Up-regulation of ZEB2 could significantly rescue the suppressive effects of miR-507 on NSCLC cells' invasion and proliferation. Conclusions: MiR-507 was noticeably downregulated in NSCLC and correlated with poor prognosis of NSCLC patients. MiR-507 represses the invasion and proliferation of NSCLC via targeting ZEB2. This study indicated that miR-507 might serve as a potential therapeutic target for NSCLC.