宫颈癌中卵泡抑素样蛋白过表达对下游基因的影响及生物信息学分析

张红; 洛若愚; 胡晓霞; 陈欢; 王琳琳

doi:10.3971/j.issn.1000-8578.2019.18.0665

宫颈癌中卵泡抑素样蛋白过表达对下游基因的影响及生物信息学分析

Effect of Overexpression of Follistatin-like Protein 1 on Downstream Genes in Cervical Cancer and Bioinformatic Analysis of Downstream Genes

摘要

摘要:
目的利用基因芯片技术对卵泡抑素样蛋白（FSTL1）下游基因及信号转导通路进行生物信息学分析，探讨FSTL1在宫颈癌中的调控机制。
方法采用基因芯片筛选转染FSTL1后HeLa细胞中的差异表达基因；运用生物信息学分析方法寻找FSTL1在宫颈癌中的差异表达基因及调控机制；用反转录实时荧光定量聚合酶链反应（RT-qPCR）对29个差异表达基因加以验证。
结果与阴性对照组相比，实验组中有881个差异表达基因，这些差异表达基因主要富集在转录调控、细胞增殖、凋亡、黏附等生物学过程以及癌症的转录误调节、丝裂源活化的蛋白激酶（MAPK）、P53等信号通路；RT-qPCR验证结果显示FSTL1上调PI3K/AKT/Bax/Bcl-2和P53信号相关通路因子，这与基因芯片结果基本符合。
结论 FSTL1的差异基因富集于转录调控、细胞增殖、凋亡、黏附等生物学过程，可能通过调控PI3K/AKT/Bax/Bcl-2和P53信号通路来参与宫颈癌的发生发展。

Abstract:
Objective To investigate the regulation mechanism of follistatin-like protein 1 (FSTL1) in cervical cancer by gene chip technology to analyze the changes of downstream genes and signaling pathways of FSTL1.
Methods The differentially-expressed genes were screened by gene chip technology in HeLa cells transfected with FSTL1. The differentially-expressed genes and regulation mechanism of FSTL1 in cervical cancer were found by bioinformatics analysis. The relative expression of 29 differentially-expressed genes were verified by real-time quantitative polymerase chain reaction (RT-qPCR).
Results Compared with the negative control group, there were 881 differentially-expressed genes in the experimental group. These differentially-expressed genes mainly enriched in the biological processes of transcription regulation, cell proliferation, apoptosis and adhesion, as well as transcription misregulation of cancer, MAPK and P53 signal pathway. RT-qPCR results showed that FSTL1 up-regulated the relevant factors of PI3K/AKT/Bax/Bcl-2 and P53 signaling pathway, which was basically consistent with the results of gene chip.
Conclusion The differentially-expressed genes of FSTL1 enrich in the biological processes of transcription regulation, cell proliferation, apoptosis and adhesion and may participate in the occurrence and development of cervical cancer by regulating PI3K/AKT/Bax/Bcl-2 and P53 signaling pathways.

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