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3 results on '"Brunet-Dunand SE"'

1. Autocrine human GH promotes radioresistance in mammary and endometrial carcinoma cells.

Author

Bougen NM, Steiner M, Pertziger M, Banerjee A, Brunet-Dunand SE, Zhu T, Lobie PE, and Perry JK

Subjects
Animals, Apoptosis drug effects, Apoptosis radiation effects, Breast Neoplasms pathology, Breast Neoplasms radiotherapy, Cell Line, Tumor, Cell Survival drug effects, Cell Survival radiation effects, DNA Damage drug effects, Endometrial Neoplasms pathology, Endometrial Neoplasms radiotherapy, Female, Gene Expression Regulation, Neoplastic, Human Growth Hormone analogs & derivatives, Human Growth Hormone antagonists & inhibitors, Human Growth Hormone genetics, Human Growth Hormone pharmacology, Humans, Mice, Radiation Tolerance drug effects, Radiation, Ionizing, Radiation-Protective Agents pharmacology, Tumor Burden drug effects, Xenograft Model Antitumor Assays, Breast Neoplasms metabolism, Endometrial Neoplasms metabolism, Human Growth Hormone metabolism, Radiation Tolerance physiology
Abstract

Although recent advances in breast cancer treatment regimes have improved patient prognosis, resistance to breast cancer therapies, such as radiotherapy, is still a major clinical challenge. In the current study, we have investigated the role of autocrine human GH (hGH) in resistance to ionising radiation (IR)-based therapy. Cell viability and total cell number assays demonstrated that autocrine hGH promoted cell regrowth in the mammary carcinoma cell lines, MDA-MB-435S and T47D, and the endometrial carcinoma cell line, RL95-2, following treatment with IR. In addition, autocrine hGH enhanced MDA-MB-435S and T47D cell clonogenic survival following radiation exposure. The enhanced clonogenic survival afforded by autocrine hGH was mediated by JAK2 and Src kinases. Investigation into the DNA repair capacity demonstrated that autocrine hGH reduced IR-induced DNA damage in MDA-MB-435S and T47D cells. Functional antagonism of hGH increased RL95-2 sensitivity to IR in cell viability and total cell number assays, reduced clonogenic survival and enhanced the induction of DNA damage. Thus, autocrine hGH reduced sensitivity to treatment with IR in mammary and endometrial carcinoma cell lines in vitro, while functional antagonism of hGH sensitised endometrial carcinoma cells to IR. Functional antagonism of hGH, used in conjunction with radiotherapy, may therefore enhance treatment efficacy and improve the prognosis of patients with breast and endometrial cancer.

Published
2012
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2. PAX5alpha enhances the epithelial behavior of human mammary carcinoma cells.

Author

Vidal LJ, Perry JK, Vouyovitch CM, Pandey V, Brunet-Dunand SE, Mertani HC, Liu DX, and Lobie PE

Subjects
Biomarkers metabolism, Breast Neoplasms genetics, Breast Neoplasms pathology, Carcinoma genetics, Carcinoma pathology, Cell Count, Cell Differentiation genetics, Cell Line, Tumor, Cell Movement genetics, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic metabolism, Down-Regulation genetics, Epithelial Cells cytology, Female, Gene Expression Regulation, Neoplastic genetics, Humans, Intercellular Junctions metabolism, Intercellular Junctions ultrastructure, Mesoderm cytology, Mesoderm metabolism, Neoplasm Invasiveness genetics, Neoplasm Invasiveness physiopathology, PAX5 Transcription Factor genetics, RNA Interference physiology, RNA, Messenger metabolism, Tumor Suppressor Proteins genetics, beta Catenin metabolism, Breast Neoplasms metabolism, Carcinoma metabolism, Cell Dedifferentiation physiology, Epithelial Cells metabolism, PAX5 Transcription Factor metabolism, Tumor Suppressor Proteins metabolism
Abstract

Deregulated PAX5 expression has been associated with metastatic mammary carcinoma, although the precise role of PAX5 in cancer progression is unclear. Stable forced expression of PAX5alpha in the mammary carcinoma cell lines MCF-7 and MDA-MB-231 reduced cell cycle progression, cell survival, and anchorage-independent cell growth. In xenograft studies, forced expression of PAX5alpha was associated with a significant reduction in tumor volume. Furthermore, forced expression of PAX5alpha in mammary carcinoma cells resulted in altered cell morphology with resultant enhancement of epithelial cell characteristics. Morphologic changes were associated with localization of beta-CATENIN at cell-cell junctions and with altered mRNA expression of mesenchymal markers in mammary carcinoma cells. In addition, forced expression of PAX5alpha in MCF-7 and MDA-MB-231 cells significantly reduced cell migration and invasion. Concomitantly, small interfering RNA-mediated depletion of PAX5alpha increased MCF-7 total cell number, cell motility, migration, and invasion. These studies show that PAX5alpha enhances the epithelial characteristics of mammary carcinoma cells, reminiscent of mesenchymal to epithelial transition.

Published
2010
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3. Autocrine human growth hormone promotes tumor angiogenesis in mammary carcinoma.

Author

Brunet-Dunand SE, Vouyovitch C, Araneda S, Pandey V, Vidal LJ, Print C, Mertani HC, Lobie PE, and Perry JK

Subjects
Breast Neoplasms genetics, Breast Neoplasms metabolism, Breast Neoplasms pathology, Carcinoma genetics, Carcinoma metabolism, Carcinoma pathology, Carrier Proteins genetics, Carrier Proteins metabolism, Cell Cycle drug effects, Cell Movement drug effects, Cell Proliferation drug effects, Endothelial Cells drug effects, Endothelial Cells metabolism, Endothelial Cells pathology, Gene Expression Regulation, Neoplastic drug effects, Human Growth Hormone genetics, Human Growth Hormone metabolism, Humans, Lymphangiogenesis drug effects, Lymphangiogenesis genetics, Neoplasm Invasiveness, Neovascularization, Pathologic genetics, Tumor Cells, Cultured, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Autocrine Communication physiology, Breast Neoplasms blood supply, Carcinoma blood supply, Human Growth Hormone pharmacology, Neovascularization, Pathologic chemically induced
Abstract

Accumulating literature implicates pathological angiogenesis and lymphangiogenesis as playing key roles in tumor progression. Autocrine human growth hormone (hGH) is a wild-type orthotopically expressed oncogene for the human mammary epithelial cell. Herein we demonstrate that autocrine hGH expression in the human mammary carcinoma cell line MCF-7 stimulated the survival, proliferation, migration, and invasion of a human microvascular endothelial cell line (HMEC-1). Autocrine/paracrine hGH secreted from mammary carcinoma cells also promoted HMEC-1 in vitro tube formation as a consequence of increased vascular endothelial growth factor-A (VEGF-A) expression. Semiquantitative RT-PCR analysis demonstrated that HMEC-1 cells express both hGH and the hGH receptor (hGHR). Functional antagonism of HMEC-1-derived hGH reduced HMEC-1 survival, proliferation, migration/invasion, and tube formation in vitro. Autocrine/paracrine hGH secreted by mammary carcinoma cells increased tumor blood and lymphatic microvessel density in a xenograft model of human mammary carcinoma. Autocrine hGH is therefore a potential master regulator of tumor neovascularization, coordinating two critical processes in mammary neoplastic progression, angiogenesis and lymphangiogenesis. Consideration of hGH antagonism to inhibit angiogenic processes in mammary carcinoma is therefore warranted.

Published
2009
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