CircRNA fibroblast growth factor receptor 3 promotes tumor progression in non-small cell lung cancer by regulating Galectin-1-AKT/ERK1/2 signaling
CircRNA fibroblast growth factor receptor 3 promotes tumor progression in non-small cell lung cancer by regulating Galectin-1-AKT/ERK1/2 signaling
复制标题
CircRNA成纤维细胞生长因子受体3通过调节半乳糖凝集素-1-AKT/ERK1/2信号促进非小细胞肺癌的肿瘤进展
DOI：
10.1002/jcp.27783
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发表时间：
2019-07-01
影响因子：
5.6
通讯作者：
Wu, Yong-Bing
中科院分区：
文献类型：
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作者：
Qiu, Bai-Quan;Zhang, Peng-Fei;Wu, Yong-Bing
环状RNA(CircRNA)表达失调参与了包括非小细胞肺癌(NSCLC)在内的多种癌症的发生发展。然而，CircRNA FGFR3(CircFGFR3)在非小细胞肺癌进展中的作用和潜在的分子机制仍不清楚。在这里，我们使用实时定量聚合酶链式反应来验证CircFGFR3在NSCLC组织中的表达高于在癌旁组织中的表达。此外，我们的研究表明，强制表达CircFGFR3促进了NSCLC细胞的侵袭和增殖。在机制上，我们发现CircFGFR3通过与miR-22-3p竞争性结合促进Galectin-1(Gal-1)、p-AKT和p-ERK1/2的表达，从而促进NSCLC细胞的侵袭和增殖。临床上，我们发现FGFR3的高表达与非小细胞肺癌患者不良的临床预后有关。总之，这些数据为FGFR3通过海绵化miR-22-3p和增加Gal-1表达对AKT和ERK1/2信号通路的调控提供了机械性的见解。
The dysregulation of circular RNA (circRNA) expression is involved in the progression of several cancers, including non-small cell lung cancer (NSCLC). However, the role and underlying molecular mechanisms of circRNA FGFR3 (circFGFR3) in NSCLC progression remains unknown. Here, we used quantitative real-time polymerase chain reaction to validate that circFGFR3 expression was higher in NSCLC tissues than in the paratumor tissues. Furthermore, our study indicated that the forced circFGFR3 expression promoted NSCLC cell invasion and proliferation. Mechanistically, we found that circFGFR3 promoted NSCLC cell invasion and proliferation via competitively combining with miR-22-3p to facilitate the galectin-1 (Gal-1), p-AKT, and p-ERK1/2 expressions. Clinically, we revealed that the high circFGFR3 expression correlates with the poor clinical outcomes in patients with NSCLC. Together, these data provide mechanistic insights into the circFGFR3-mediated regulation of both the AKT and ERK1/2 signaling pathways by sponging miR-22-3p and increasing Gal-1 expression.