Abstract
We recently discovered a novel gene responsive to tumor-conditioned media: endothelial-derived gene 1 (EG-1). Its transcript has been shown to be present in epithelial cells, as well as in endothelial cells. In this study, we examined the levels of EG-1 protein expression in breast, colon, prostate, and lung cancers, which constitute the four most common solid malignancies in the United States. Polyclonal antibodies were generated that recognize the EG-1 peptide. These antibodies were used in immunoblot analysis, as well as immunohistochemistry of multiple human clinical specimens of cancer. In immunoblots of whole cell lysates, EG-1 antibodies revealed the presence of a 22-kDa peptide. Immunohistochemistry of breast, colon, and prostate specimens showed higher levels of EG-1 peptides in cancer tissues, in comparison with their benign counterparts. However, EG-1 expression was minimal in both benign and malignant lung tissues. Here, we demonstrated that the expression of EG-1 is elevated in cancerous in comparison to benign epithelial cells, as seen in immunohistochemistry of human pathological specimens. These observations collectively support the hypothesis that the novel gene EG-1 is associated with the malignant phenotype of the common epithelial-derived cancers of the breast, colon, and prostate.
Highlights
Cancer is a major cause of morbidity and the second leading cause of death in the American population
In immunoblots of whole cell lysates, endothelial-derived gene 1 (EG-1) antibodies revealed the presence of a 22-kDa peptide
Here, we demonstrated that the expression of EG-1 is elevated in cancerous in comparison to benign epithelial cells, as seen in immunohistochemistry of human pathological specimens
Summary
Cancer is a major cause of morbidity and the second leading cause of death in the American population. Several major oncogenes and tumor suppressor genes have been identified to contribute to the neoplastic transformation of epithelial cells. These include p53, c-myc, ras, retinoblastoma, BRCA-1 and BRCA-2 (breast cancer susceptibility genes), Her-2, cyclin D1, and phosphatase and tensin homologue [2]. Other alterations in the cell such as DNA methylation contribute to the overall genetic instability, whereas abnormal maintenance of telomerases results in replicative immortality [3]. Another important biological phenomenon in the tumorigenic and metastatic phenotype involves the process of angiogenesis. Abnormal angiogenesis occurs in rheumatoid arthritis, diabetic retinopathy, and in cancer growth and metastasis
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