Objective. To study the expression, biological function, and mechanism of FKBP4 in non-small-cell lung cancer (NSCLC). Methods. First of all, the expression of FKBP4 in NSCLC tissues and cell lines was detected by qRT-PCR; then, the effects of FKBP4 on proliferation, apoptosis, migration, and invasion of NSCLC were studied by CCK-8 assays, flow cytometry assays, wound-healing assays, and Transwell assays. After that, tumor xenografts were used to explore the effect of FKBP4 on NSCLC tumor growth in vivo, and the phosphorylation of Akt and mTOR was measured by western blot. Results. FKBP4 was highly expressed in NSCLC tissues and cells, and its expression was closely related to NSCLC tumor size, lymph node metastasis, and patient prognosis. In vitro, FKBP4 can promote NSCLC cell proliferation, migration, and invasion and inhibit NSCLC cell apoptosis. In vivo, FKBP4 can promote NSCLC tumor growth. Furthermore, FKBP4 can promote Akt and mTOR phosphorylation and activate the Akt/mTOR signaling pathway and an mTOR inhibitor can neutralize the functions of FKBP4 in NSCLC cells. Conclusion. FKBP4 serves as an oncogene to promote malignant processes in NSCLC, and it has the potential to be used as a biological marker and therapeutic target for NSCLC.

中文翻译：

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FKBP4 通过激活 Akt/mTOR 信号通路加速非小细胞肺癌的恶性进展

客观。研究FKBP4在非小细胞肺癌（NSCLC）中的表达、生物学功能及机制。方法。首先通过qRT-PCR检测FKBP4在NSCLC组织和细胞系中的表达；然后，通过CCK-8测定、流式细胞术测定、伤口愈合测定和Transwell测定研究了FKBP4对NSCLC增殖、凋亡、迁移和侵袭的影响。之后，使用肿瘤异种移植物来探索FKBP4对体内NSCLC肿瘤生长的影响，并通过蛋白质印迹法测量Akt和mTOR的磷酸化。结果. FKBP4在NSCLC组织和细胞中高表达，其表达与NSCLC肿瘤大小、淋巴结转移及患者预后密切相关。在体外，FKBP4可以促进NSCLC细胞增殖、迁移和侵袭，抑制NSCLC细胞凋亡。在体内，FKBP4 可以促进 NSCLC 肿瘤的生长。此外，FKBP4 可以促进 Akt 和 mTOR 磷酸化并激活 Akt/mTOR 信号通路，mTOR 抑制剂可以中和 FKBP4 在 NSCLC 细胞中的功能。结论。FKBP4作为促进NSCLC恶性进程的癌基因，具有作为NSCLC的生物学标志物和治疗靶点的潜力。