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

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/A