Department of Thoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Department of Gastroenterology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
J Biochem. 2022 Feb 21;171(2):245-252. doi: 10.1093/jb/mvab129.
Non-small cell lung cancer (NSCLC) has markedly increased morbidity and mortality rates worldwide. Circular RNAs were shown to regulate NSCLC progression. But the underlying pathways of the circRPPH1-mediated regulation of NSCLC still need further exploration. We evaluated circRPPH1 levels in NSCLC tissues and cell lines via qRT-PCR. Moreover, using ectopic plasmid incorporation and siRNA assays, we analysed the circRPPH1-mediated regulation of cell proliferation (CP), cell migration (CM) and cell invasion (CI) in NSCLC cell lines (H1975 and A549 cells), using CCK-8, colony forming, scratch wound and transwell assays, respectively. CircRPPH1 levels were remarkably high in the NSCLC tissues and cell lines. The transfection experiments showed that circRPPH1 overexpression was able to promote CP, CM and CI of NSCLC cells, while CP, CM and CI were significantly restrained by the knockdown of circRPPH1. We also displayed that circRPPH1 knockdown suppressed the cell progression via inactivating the PI3K/AKT and JAK2/STAT3 signalling axes. Subsequently, in vivo experiment in nude mice was demonstrated that the inhibition of circRPPH1 could reduce the tumour growth of NSCLC. circRPPH1 may accelerate the growth and metastasis of NSCLC, in culture conditions and in animal models, by stimulating the PI3K/AKT and JAK2/STAT3 signalling axes, thus promoting the development of NSCLC.
非小细胞肺癌（NSCLC）在全球范围内的发病率和死亡率显著增加。环状 RNA 被证明可以调节 NSCLC 的进展。但是，circRPPH1 介导的 NSCLC 调节的潜在途径仍需要进一步探索。我们通过 qRT-PCR 评估了 NSCLC 组织和细胞系中的 circRPPH1 水平。此外，我们使用外源性质粒掺入和 siRNA 测定，分别通过 CCK-8、集落形成、划痕伤口和 Transwell 测定分析了 circRPPH1 对 NSCLC 细胞系（H1975 和 A549 细胞）中细胞增殖（CP）、细胞迁移（CM）和细胞侵袭（CI）的调节作用。circRPPH1 水平在 NSCLC 组织和细胞系中显著升高。转染实验表明，circRPPH1 过表达能够促进 NSCLC 细胞的 CP、CM 和 CI，而 circRPPH1 的敲低则显著抑制 CP、CM 和 CI。我们还显示，circRPPH1 敲低通过抑制 PI3K/AKT 和 JAK2/STAT3 信号通路来抑制细胞进展。随后，裸鼠体内实验表明，抑制 circRPPH1 可以减少 NSCLC 的肿瘤生长。circRPPH1 可能通过刺激 PI3K/AKT 和 JAK2/STAT3 信号通路，在培养条件下和动物模型中加速 NSCLC 的生长和转移，从而促进 NSCLC 的发展。
