Abstract：
BACKGROUND: The intricate biological mechanism underlying lung adenocarcinoma (LUAD), characterized by a deficiency of distinctive biomarkers, remain elusive. The presence of Long non-coding RNAs (lncRNAs) have been established to play a role in carcinogenesis. Nevertheless, the regulatory effects and mechanisms of lncRNA CYTOR in LUAD have yet to be elucidated.
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.
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.
摘要：
背景：肺腺癌（LUAD）的复杂生物学机制，以缺乏独特的生物标志物为特征，仍然难以捉摸。长非编码RNA（lncRNA）的存在已被确定为在癌发生中起作用。然而，lncRNACYTOR在LUAD中的调节作用和机制尚未阐明。
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。
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。
