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Soy peptide up-regulates tumor suppressor and other chemopreventive genes in prostate epithelial cells

ABSTRACT: Numerous studies have identified certain components of soybean as having anticancer properties. Lunasin, a unique 43-amino acid soybean peptide, has been shown to suppress carcinogenesis in mammalian cells and mouse models. It has been hypothesized that lunasin modulates changes in chromatin organization by modifying histone tails, thereby, resulting in the expression of chemopreventive genes. In this report, microarray analysis was used to reveal a novel property of lunasin – its ability to up-regulate tumor suppressor and other chemopreventive genes in prostate epithelial cells. The effects of exogenous lunasin on the comprehensive gene expression profiles revealed that a total of 123 genes had a greater than twofold change in expression in the lunasin-treated cells as compared to the mock-treated cells. Of these genes, 121 genes were up-regulated in normal RWPE-1 cells and only two genes were up-regulated in malignant RWPE-2 epithelial cells. The genes up-regulated in RWPE-1 cells include those involved in tumor suppression, apoptosis, and the control of cell division. The results shed new light on lunasin’s previously observed chemopreventive properties. We propose that lunasin prevents cancer in vitro and in small animal models by up-regulating the expression of genes that prevent the onset of the disease. Keywords: treatment with lunasin soy peptide

ORGANISM(S): Homo sapiens

PROVIDER: GSE2992 | GEO | 2005/07/26

SECONDARY ACCESSION(S): PRJNA91947

REPOSITORIES: GEO

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Project description:Purpose: Chronic pulmonary inflammation in the form of chronic obstructive pulmonary disease (COPD) has been consistently shown to increase the risk of lung cancer. Therefore, identification of chemopreventive agents with anti-inflammatory effects, in addition to antiproliferative and apoptotic activities, is indispensable. Recently, we found that combinations of silibinin (Sil) and indole-3-carbinol (I3C) significantly inhibited lung tumorigenesis induced by 4-(methylnitro-samino)-1-(3-pyridyl)-1-butanone (NNK) and enhanced by chronic treatment with the inflammatory agent lipopolysaccharide (LPS). In this study, we described gene expression profiling of lung tissues using RNA-seq to determine the gene expression signature in inflammation-driven lung tumors and modulation of this signature by the chemopreventive agents Sil and I3C. Methods: Total RNA extracted from lung tissues of control and treated mice were processed for mRNA sequencing, in triplicate, using Illumina HiSeq 2000. The sequence reads that passed quality filters were analyzed for transcript abundance at the gene level using CLC Bio Genomics Workbench and differential gene expression analysis was performed using the built-in Empirical Analysis of Differential Gene Expression (DGE) based on 'Exact Test' method. qRTâPCR validation was performed using SYBR Green assays. Results and conclusions: We found that 330, 2,957, and 1,143 genes were differentially regulated in mice treated with NNK, LPS, and NNK + LPS, respectively. The expression of inflammation-and immunity-related genes was significantly more deregulated in lung tissues of mice treated with LPS alone compared to mice treated with NNK + LPS. Among 1,143 genes differentially regulated in the NNK + LPS group, the expression of 162 genes and associated signaling pathways were significantly modulated by I3C and/or Sil + I3C. These genes include cytokines, chemokines, and genes with a well-established role in inflammation and/or tumorigenesis such as c-ros oncogene 1 (Ros1), the EGFR ligands amphiregulin and epiregulin, Cyp1a1, and the circadian rhythm genes Arntl, and Npas2. To our knowledge, this is the first report that provides insight into genes that are differentially expressed during inflammation-driven lung tumorigenesis and the modulation of these genes by chemopreventive agents. Lung tissue mRNA profiles of mice treated with control vehicle, NNK, LPS, NNK+LPS, or NNK+LPS supplemented with chemopreventive agent(s) were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.

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Soy peptide up-regulates tumor suppressor and other chemopreventive genes in prostate epithelial cells

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