Department of Respiratory Medicine, Maoming People's Hospital, Maoming, China.
Eur Rev Med Pharmacol Sci. 2019 Nov;23(22):9955-9964. doi: 10.26355/eurrev_201911_19562.
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.
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).
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.
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.
非小细胞肺癌（NSCLC）是全球最常见的恶性肿瘤之一，目前仍在探索有效的治疗方法。miR-507 在某些类型的癌症中存在异常表达，并影响癌细胞行为。然而，miR-507 在 NSCLC 中的作用尚不清楚。本研究旨在探讨 miR-507 在 NSCLC 中的表达、生物学功能及其作用机制。
采用实时定量 PCR（qRT-PCR）检测 NSCLC 组织和细胞系中 miR-507 的表达。采用细胞计数试剂盒-8（CCK-8）和集落形成实验检测 NSCLC 细胞的增殖能力。Transwell 实验检测 NSCLC 细胞的侵袭能力。双荧光素酶报告实验验证 miR-507 与锌指 E 盒结合同源盒 2（ZEB2）之间的结合。
miR-507 在 NSCLC 组织和细胞系中表达下调。miR-507 低表达与 NSCLC 患者预后不良相关。过表达 miR-507 抑制 NSCLC 细胞侵袭和增殖。ZEB2 被预测为 miR-507 的直接下游分子，双荧光素酶报告实验验证了它们之间的直接结合。上调 ZEB2 可显著挽救 miR-507 对 NSCLC 细胞侵袭和增殖的抑制作用。
miR-507 在 NSCLC 中明显下调，与 NSCLC 患者的不良预后相关。miR-507 通过靶向 ZEB2 抑制 NSCLC 的侵袭和增殖。本研究表明，miR-507 可能成为 NSCLC 的潜在治疗靶点。
