miR-496 通过靶向 BDNF 介导的 PI3K/Akt 信号通路抑制非小细胞肺癌的肿瘤发生。
miR-496 suppress tumorigenesis via targeting BDNF-mediated PI3K/Akt signaling pathway in non-small cell lung cancer.
机构信息
Department of Integrated Medicine, Affiliated to Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
Department of Laboratory Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
出版信息
Biochem Biophys Res Commun. 2019 Oct 15;518(2):273-277. doi: 10.1016/j.bbrc.2019.08.046. Epub 2019 Aug 14.
microRNA-496 (miR-496) was found expressed abnormally in non-small cell lung cancer (NSCLC). But the study about the role of miR-496 on NSCLC was not satisfactory in date. Therefore, here we designed to explore the role of miR-496 and the probable internal mechanism in tumorigenesis of NSCLC. Increasing miR-496 both in NSCLC patients and cell lines could significantly restrained cell proliferation. For farther researching the regulation mechanism of miR-496 on NSCLC, we screen Brain derived neurotrophic factor (BDNF) as a potential target of miR-496 by bioinformatic methods and predicted a possible target of miR-496 in the 3'untranslated region (UTR) of miR-496. In clinical patients and most NSCLC cell lines including H1650, H292, H1944 and A549, increasing expression of miR-496 suppressed tumor growth via inactivating BDNF-mediated PI3K/Akt signaling pathway activation. In a word, our fingdings first represent a mechanism of miR-496 on NSCLC tumor growth via inactivating BDNF-mediated PI3K/Akt signaling pathway.
微小 RNA-496（miR-496）在非小细胞肺癌（NSCLC）中表达异常。但是，目前关于 miR-496 在 NSCLC 中的作用的研究还不尽人意。因此，我们设计在这里探讨 miR-496 在 NSCLC 发生中的作用及其可能的内在机制。在 NSCLC 患者和细胞系中增加 miR-496 的表达可以显著抑制细胞增殖。为了进一步研究 miR-496 对 NSCLC 的调控机制，我们通过生物信息学方法筛选脑源性神经营养因子（BDNF）作为 miR-496 的潜在靶标，并预测 miR-496 在 miR-496 的 3'非翻译区（UTR）中的一个可能靶标。在临床患者和大多数 NSCLC 细胞系中，包括 H1650、H292、H1944 和 A549，增加 miR-496 的表达通过抑制 BDNF 介导的 PI3K/Akt 信号通路的激活来抑制肿瘤生长。总之，我们的研究结果首次代表了 miR-496 通过抑制 BDNF 介导的 PI3K/Akt 信号通路来抑制 NSCLC 肿瘤生长的机制。
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