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microRNA-30b 通过靶向表皮生长因子受体抑制非小细胞肺癌细胞生长。

MicroRNA-30b inhibits non-small cell lung cancer cell growth by targeting the epidermal growth factor receptor.

出版信息

Neoplasma. 2018;65(2):192-200. doi: 10.4149/neo_2018_170217N118.

DOI:10.4149/neo_2018_170217N118
PMID:29534579
Abstract

Lung cancer, especially non-small cell lung cancer (NSCLC), is the leading cause of cancer-related mortality in the world. Both microRNAs and epidermal growth factor receptor (EGFR) are important factors in NSCLC. In our study, the expression of miR-30b in 47 tumor tissues and paired normal tissues of NSCLC were detected by RT-PCR, and we found that miR-30b was down-regulated in NSCLC tumor tissues and was associated with TNM stage, differentiation, and lymph node metastases. Then we investigated the ability of miR-30b to regulate EGFR in several NSCLC cell lines, and found that miR-30b inhibited proliferation, migration and invasion, induced apoptosis and enhanced sensitivity of the NSCLC cells to EGFR tyrosine kinase inhibitors (EGFR-TKIs) by targeting EGFR and repressing EGFR signaling pathways. Overall, these results indicate that miR-30b may be a potential therapeutic target in NSCLC patients.

摘要

肺癌,尤其是非小细胞肺癌(NSCLC),是全球癌症相关死亡的主要原因。microRNAs 和表皮生长因子受体(EGFR)都是 NSCLC 的重要因素。在我们的研究中,通过 RT-PCR 检测了 47 例 NSCLC 肿瘤组织和配对正常组织中 miR-30b 的表达,我们发现 miR-30b 在 NSCLC 肿瘤组织中下调,并与 TNM 分期、分化和淋巴结转移相关。然后,我们研究了 miR-30b 在几种 NSCLC 细胞系中调节 EGFR 的能力,发现 miR-30b 通过靶向 EGFR 并抑制 EGFR 信号通路,抑制增殖、迁移和侵袭,诱导细胞凋亡,并增强 NSCLC 细胞对 EGFR 酪氨酸激酶抑制剂(EGFR-TKIs)的敏感性。总的来说,这些结果表明 miR-30b 可能是 NSCLC 患者的一个潜在治疗靶点。

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