Abstract
Prostate cancer caused by the abnormal disorderly growth of prostatic acinar cells is the most prevalent cancer of men in western countries. We aimed to screen out differentially expressed genes (DEGs) and explore small molecule drugs for prostate cancer. The GSE3824 gene expression profile of prostate cancer was downloaded from Gene Expression Omnibus database which including 21 normal samples and 18 prostate cancer cells. The DEGs were identified by Limma package in R language and gene ontology and pathway enrichment analyses were performed. In addition, potential regulatory microRNAs and the target sites of the transcription factors were screened out based on the molecular signature database. In addition, the DEGs were mapped to the connectivity map database to identify potential small molecule drugs. A total of 6,588 genes were filtered as DEGs between normal and prostate cancer samples. Examples such as ITGB6, ITGB3, ITGAV and ITGA2 may induce prostate cancer through actions on the focal adhesion pathway. Furthermore, the transcription factor, SP1, and its target genes ARHGAP26 and USF1 were identified. The most significant microRNA, MIR-506, was screened and found to regulate genes including ITGB1 and ITGB3. Additionally, small molecules MS-275, 8-azaguanine and pyrvinium were discovered to have the potential to repair the disordered metabolic pathways, abd furthermore to remedy prostate cancer. The results of our analysis bear on the mechanism of prostate cancer and allow screening for small molecular drugs for this cancer. The findings have the potential for future use in the clinic for treatment of prostate cancer.
Highlights
As a kind of malignancy, prostate cancer is resulting from the pathological changes in men’s prostate tissue (DeMarzo et al, 2003)
Language, at a p-value of 0.05, a total of 10611 probes were identified to be differentially expressed in prostate cancer samples compared with normal controls, which corresponded to 6588 differentially expressed genes (DEGs)
A total of 6588 DEGs were identified between prostate cancer samples and normal controls
Summary
As a kind of malignancy, prostate cancer is resulting from the pathological changes in men’s prostate tissue (DeMarzo et al, 2003). Considerable researches are undertaken around prostate cancer. The researches about the molecular genetics and growth regulation of the prostate cancer have made remarkable progress (Singh et al, 2012). Abundant of reports about the regulatory functions of transcription factors and microRNAs in cancer have been published. They mostly focused on a certain target or DNA. There are some small molecules which can treat prostate cancer, such as CPIC (1-(3-(2-chlorophenoxy) propyl)1H-indole-3-carbonitrile), AR54 ((2-(pyrimidin-2ylthio)-1-(2,2,4-trimethyl-4-phenyl-3,4-dihydroquinolin1(2H)-yl)ethanone) (Shapiro et al, 2012). These molecules don’t treat the prostate cancer efficiently and selectively. The need for new methods to elucidate the mechanism of prostate cancer and new therapeutics for prostate cancer is highlighted
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