The abnormal expression of follistatin‑like protein 1 (FSTL1) in various tumors is a crucial regulator of the biological process of tumorigenesis. Nonetheless, the regulatory role of FSTL1 in cervical cancer is yet to be elucidated. Hence, the present study aimed to explore the expression, function, and molecular mechanism of FSTL1 in cervical cancer. The expression of FSTL1 in normal and cervical cancer tissues was examined using quantitative reverse transcription‑polymerase chain reaction and immunohistochemistry assays. The effects of abnormal expression of FSTL1 on cervical cancer cells were assessed using colony formation, MTT, wound‑healing, Transwell, apoptosis, and nude mouse tumorigenicity assays. FSTL1‑related molecular mechanisms were screened using gene chip analysis. Western blotting analysis was used to verify the regulatory mechanisms of FSTL1 in cervical cancer. The results indicated that the expression of FSTL1 was downregulated in cervical cancer tissues and that its downregulation was associated with tumor differentiation, pathologic type, and infiltration depth. Moreover, FSTL1 inhibited the proliferation, migration, and invasion of cervical cancer cells as well as xenograft tumor growth and promoted cell apoptosis. In addition, the findings of gene chip analysis suggested that the differentially expressed genes of FSTL1 were predominantly enriched in multiple signaling pathways, of which the insulin‑like growth factor (IGF)‑1 signaling pathway was significantly activated. Western blotting suggested the involvement of FSTL1 in the regulation of the IGF‑1R/PI3K/AKT/BCL‑2 signaling pathway. These data establish the downregulation of FSTL1 in cervical cancer tissues. FSTL1 inhibited the proliferation, migration, and invasion of cervical cancer cells and promoted their apoptosis. Furthermore, xenograft tumor growth in nude mice was inhibited. FSTL1 may be involved in the regulation of the IGF‑1R/PI3K/AKT/BCL‑2 signaling pathway in cervical cancer. Therefore, FSTL1 may be employed as a novel biomarker to determine the extent of disease progression in patients with cervical cancer.

中文翻译：

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卵泡抑素样蛋白1在宫颈癌中的表达及机制分析

卵泡抑素样蛋白1（FSTL1）在多种肿瘤中的异常表达是肿瘤发生生物学过程的重要调节因子。尽管如此，FSTL1在宫颈癌中的调节作用尚未阐明。因此，本研究旨在探讨FSTL1在宫颈癌中的表达、功能及其分子机制。使用定量逆转录聚合酶链反应和免疫组织化学分析检测正常组织和宫颈癌组织中 FSTL1 的表达。使用集落形成、MTT、伤口愈合、Transwell、细胞凋亡和裸鼠致瘤性测定来评估 FSTL1 异常表达对宫颈癌细胞的影响。使用基因芯片分析筛选 FSTL1 相关分子机制。采用Western blotting分析验证FSTL1在宫颈癌中的调控机制。结果表明，FSTL1在宫颈癌组织中表达下调，且其表达下调与肿瘤分化程度、病理类型、浸润深度相关。此外，FSTL1抑制宫颈癌细胞的增殖、迁移和侵袭以及异种移植肿瘤的生长并促进细胞凋亡。此外，基因芯片分析结果表明，FSTL1的差异表达基因主要富集于多个信号通路，其中胰岛素样生长因子（IGF）-1信号通路显着激活。蛋白质印迹表明 FSTL1 参与 IGF-1R/PI3K/AKT/BCL-2 信号通路的调节。这些数据证实了宫颈癌组织中 FSTL1 的下调。FSTL1抑制宫颈癌细胞的增殖、迁移和侵袭并促进其凋亡。此外，裸鼠体内异种移植肿瘤的生长也受到抑制。FSTL1可能参与宫颈癌IGF-1R/PI3K/AKT/BCL-2信号通路的调节。因此，FSTL1可以作为一种新的生物标志物来确定宫颈癌患者疾病进展的程度。