Tissue-Specific Pathways for Estrogen Regulation of Ovarian Cancer Growth and Metastasis

Menopausal estrogen (E2) replacement therapy increases the risk of estrogen receptor (ER)-positive epithelial ovarian cancers (EOC). Whether E2 is tumorigenic or promotes expansion of undiagnosed preexisting disease is unknown. To determine E2 effects on tumor promotion, we developed an intraperiton...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2010-11, Vol.70 (21), p.8927-8936
Main Authors: SPILLMAN, Monique A, MANNING, Nicole G, DYE, Wendy W, SARTORIUS, Carol A, POST, Miriam D, CHUCK HARRELL, Joshua, JACOBSEN, Britta M, HORWITZ, Kathryn B
Format: Article
Language:English
Subjects:
Animals
Antineoplastic agents
Biological and medical sciences
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Blotting, Western
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cell Line, Tumor
Cell Proliferation
Estrogens - pharmacology
Female
Female genital diseases
Gene Expression Profiling
Gene Expression Regulation, Neoplastic - drug effects
Gynecology. Andrology. Obstetrics
Humans
Immunoenzyme Techniques
Lymphatic Metastasis
Medical sciences
Mice
Mice, Nude
Oligonucleotide Array Sequence Analysis
Organ Specificity
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - genetics
Ovarian Neoplasms - pathology
Peritoneal Neoplasms - drug therapy
Peritoneal Neoplasms - genetics
Peritoneal Neoplasms - secondary
Pharmacology. Drug treatments
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
Selective Estrogen Receptor Modulators - pharmacology
Tumors
Xenograft Model Antitumor Assays
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Summary:Menopausal estrogen (E2) replacement therapy increases the risk of estrogen receptor (ER)-positive epithelial ovarian cancers (EOC). Whether E2 is tumorigenic or promotes expansion of undiagnosed preexisting disease is unknown. To determine E2 effects on tumor promotion, we developed an intraperitoneal mouse xenograft model using ZsGreen fluorescent ER(-) 2008 and ER(+) PEO4 human EOC cells. Tumor growth was quantified by in vivo fluorescent imaging. In ER(+) tumors, E2 significantly increased size, induced progesterone receptors, and promoted lymph node metastasis, confirming that ERs are functional and foster aggressiveness. Laser-captured human EOC cells from ER(-) and ER(+) xenografted tumors were profiled for expression of E2-regulated genes. Three classes of E2-regulated EOC genes were defined, but
ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.CAN-10-1238