GSE128131
C89 Induces the autophagy of Female Germline Stem cells Via inhibition of PI3K-AKT Signaling Pathway in vitro
Purpose: To uncover the mechanism of C89-induced autophagy in FGSCs, we used RNA sequencing technology to compare the mRNA expression differences between the control groups and the C89 treated groups. FGSCs mRNA profiles of the control groups and the C89 treated groups were generated by deep sequencing, in triplicate. The library quality was determined using a Bioanalyzer 2100 (Agilent). The Illumina HiSeq 2500 platform was used for RNA sequencing. The quality of RNA-seq reads was examined using FastQC. Using an optimized data analysis workflow, we identified 15243 transcripts in the FGSCs of the control groups and the C89 treated groups. After applying a stringent filtering approach that compared control and C89-treated groups (adjusted p value, < 0.05; fold change, > 1.5 or < 0.5), we identified 937 upregulated and 1046 downregulated mRNAs. Approximately 13% of the transcripts showed differential expression between the control and C89-treated groups, with a fold change =1.5 and p value <0.05.And we found 4 differentially expressed mRNAs was related to autophagy and qRT-PCR was used to verify it. The GO and KEGG analyse reveal that the differential expression mRNAs were related to the process of cell proliferation, death and immunoreaction. Our study analyse of the control groups and the C89 treated groups transcriptomes, with biologic functions, generated by RNA-seq technology.The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that the PI3K-AKT pathway was related to the influence of C89 on FGSCs. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions. Overall design: C89-treated and control FGSCs mRNA profiles of 8h were generated by deep sequencing, in triplicate.