METHODS: In this study, RT-qPCR and Western blot were adopted to examine gene mRNA and protein expression, respectively. Cell proliferation was evaluated by CCK-8 assays. Transwell was performed to assay cell migration and invasion. The function of CYTOR in vivo was investigated through a xenograft animal model.
RESULTS: We observed an apparent upregulation of CYTOR in LUAD. Silencing CYTOR significantly reduced proliferation, migration, and invasion capabilities of LUAD cells. Mechanism analysis indicated that CYTOR targeted the miR-503-5p/PCSK9 axis. Additionally, inhibiting of miR-503-5p partially reversed the inhibitory effects of CYTOR silencing on the malignant progression of LUAD cells. Animal experiments revealed that CYTOR/miR-503-5p/PCSK9 curbed tumor formation of nude mice in vivo.
CONCLUSIONS: These findings demonstrated that lncRNA CYTOR acted as an oncogene in LUAD, regulating tumor malignant progression through the miR-503-5p/PCSK9 axis. This study unveiled a new regulation mechanism of LUAD progression, offering potential therapeutic targets for LUAD.
方法:在本研究中,采用RT-qPCR和Westernblot检测基因mRNA和蛋白表达,分别。通过CCK-8测定评价细胞增殖。进行Transwell以测定细胞迁移和侵袭。通过异种移植动物模型研究体内CYTOR的功能。
结果:我们观察到LUAD中CYTOR的明显上调。沉默CYTOR显著减少增殖,迁移,和LUAD细胞的侵袭能力。机制分析表明CYTOR靶向miR-503-5p/PCSK9轴。此外,miR-503-5p的抑制部分逆转了CYTOR沉默对LUAD细胞恶性进展的抑制作用。动物实验表明CYTOR/miR-503-5p/PCSK9抑制了裸鼠体内肿瘤的形成。
结论:这些研究结果表明,lncRNACYTOR在LUAD中起着癌基因的作用,通过miR-503-5p/PCSK9轴调节肿瘤恶性进展。这项研究揭示了LUAD进展的新调控机制,为LUAD提供潜在的治疗靶点。