• Prostate cancer (PC) develops in the prostate (a male sex gland) and is a common malignancy and a leading cause of cancer death among men. In addition to genetic alteration, epigenetic aberration plays key roles in progression of PC. Studies in epigenetic changes in PC have accumulated vast amount of useful data that could shed light on the development of PC and include potential epigenetic markers as diagnosis and prognosis for PC. Therefore, we constructed PEpiD to store the curated epigenetic data retrieved by literature mining, which previous studies indicated as involved in PC of human, mouse, and rat. A user-friendly interface is implemented for easy and flexible query. PEpiD can serve as an important resource for epigenetic research in PC.
  • DNA methylation is a well-studied epigenetic gene regulation mechanism. DNA hypermethylation especially in the CpG island in the promoter of tumor suppressor genes causes tumorigenesis, including prostate cancer. The genes with aberrant methylation in prostate cancer involved in a number of physiological processes such as tumor-cell invasion, cell cycle control, and DNA damage repair. Hypermethylation in promoters results in inappropriate silencing of these genes and their functional loss that contributes to cancer initiation, progression, invasion, and metastasis. Some of the hypermethylated genomic loci have been used in diagnosis and therapy of prostate cancer. Therefore, the section DNA methylation in PEpiD collects genes and genomic loci with aberrant methylation involved in prostate cancer.
  • Histone modifications regulate gene expression by chromatin remodeling and recruitment of other protein factors. There are various types of histone modifications. Some are markers for gene activation. For example, trimethylation of lysine 4 on histone 3 (H3K4me3), acetylation of lysine 9 on histone 3 (H3K9ac). Some are markers for gene silencing. For example, trimethylation of lysine 27 on histone 3 (H3K27me3). Some genes involved in prostate cancer are potentially regulated by histone modification, for example, coxsackie and adenovirus receptor (CAR). Histone acetylation activates the CAR gene in the prostate cancer cell line PC-3. H3K4me may repress transcription of the prostate-specific antigen (PSA) gene in the prostate cancer cell line LNCaP. Recently, ChIP-seq/chip technology has been employed to map the genome-wide histone modifications related to prostate cancer. Therefore, the section Histone modification in PEpiD stores histone modifications involved in prostate cancer.
  • MicroRNAs are a class of short RNA molecules, ~22 nucleotides. They are post-transcriptional regulators that usually degrade target mRNAs or repress their translation by binding to complementary sequences within mRNA molecules. Generally speaking, one microRNA has multiple target mRNAs, vice versa. They form a complex regulatory network. Aberrant expression of microRNAs has been found to have links with the development of cancer including prostate cancer. Some involve in the process of Epithelial-to-Mesenchymal Transition (EMT) in PCa. Interestingly, studies have found differential expression of dozens of microRNAs between benign tumors and carcinoma tumors. Hierarchical clustering analysis accurately separated the carcinomas from the benign prostatic hyperplasia samples on the basis of their microRNA expression. This indicates that microRNAs could be potential markers for diagnosis and prognosis for prostate cancer. Therefore, the section microRNA in PEpiD stores microRNAs that published work indicated as involved in prostate cancer.