Icilin inhibits E2F1-mediated cell cycle regulatory programs in prostate cancer.
Biochem Biophys Res Commun, 2013/11/29;441(4):1005-10.
Lee S[1], Chun JN, Kim SH, So I, Jeon JH
Affiliations
PMID: 24239550
Impact factor: 3.322
Abstract
Aberrant expression of cell cycle regulators have been implicated in prostate cancer development and progression. Therefore, understanding transcriptional networks controlling the cell cycle remain a challenge in the development of prostate cancer treatment. In this study, we found that icilin, a super-cooling agent, down-regulated the expression of cell cycle signature genes and caused G1 arrest in PC-3 prostate cancer cells. With reverse-engineering and an unbiased interrogation of a prostate cancer-specific regulatory network, master regulator analysis discovered that icilin affected cell cycle-related transcriptional modules and identified E2F1 transcription factor as a target master regulator of icilin. Experimental analyses confirmed that icilin reduced the activity and expression levels of E2F1. These results demonstrated that icilin inactivates a small regulatory module controlling the cell cycle in prostate cancer cells. Our study might provide insight into the development of cell cycle-targeted cancer therapeutics.
Keywords: Bioinformatics; Gene expression profiling; Icilin; Microarray; Prostate cancer
MeSH terms
Cell Cycle; Cell Line, Tumor; DNA, Superhelical; E2F1 Transcription Factor; Humans; Male; Prostatic Neoplasms; Pyrimidinones
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