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/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.