Obesity and the associated mediators leptin, estrogen and IGF-I enhance the cell proliferation and early tumorigenesis of breast cancer cells.
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Obesity and the associated mediators leptin, estrogen and IGF-I enhance the cell proliferation and early tumorigenesis of breast cancer cells. / Lautenbach, Anne; Budde, Anne; Wrann, Christiane D; Teichmann, Birgit; Vieten, Gertrud; Karl, Tim; Nave, Heike.
in: NUTR CANCER, Jahrgang 61, Nr. 4, 4, 2009, S. 484-491.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Obesity and the associated mediators leptin, estrogen and IGF-I enhance the cell proliferation and early tumorigenesis of breast cancer cells.
AU - Lautenbach, Anne
AU - Budde, Anne
AU - Wrann, Christiane D
AU - Teichmann, Birgit
AU - Vieten, Gertrud
AU - Karl, Tim
AU - Nave, Heike
PY - 2009
Y1 - 2009
N2 - Breast cancer continues to be a major cause of cancer deaths in women. Estrogen, which is also produced by the adipose tissue, is held responsible for the elevated risk of breast cancer in obese women. However, the adipose tissue secrets hormones and adipokines such as leptin and IGF-I and these substances could also contribute to an increased breast cancer risk for obese women. In this study, the impact of obesity on cell proliferation was investigated. The carcinogen 7, 12, dimethylbenz[a]anthracene (DMBA) was administered to normal weight and diet-induced obese female Sprague-Dawley rats. Cell proliferation was evaluated by immunohistological staining of BrdU-incorporation. In the mammary glands and inguinal lymphatic nodes of the obese rats, cell proliferation was significantly increased, indicating a significant influence of obesity on breast cancer. Effects of leptin, estrogen, and IGF-I on the proliferation of MCF-7 cells in vitro were assessed using an MTT assay. Cell culture experiments demonstrated a mitogenic role of these three mediators on cell proliferation. Our data demonstrate a stimulative effect of substances produced by the adipose tissue on breast cancer. Body weight specific cell proliferation suggests that obesity-related adipokines and mediators enhance cell proliferation and increase the risk for breast cancer.
AB - Breast cancer continues to be a major cause of cancer deaths in women. Estrogen, which is also produced by the adipose tissue, is held responsible for the elevated risk of breast cancer in obese women. However, the adipose tissue secrets hormones and adipokines such as leptin and IGF-I and these substances could also contribute to an increased breast cancer risk for obese women. In this study, the impact of obesity on cell proliferation was investigated. The carcinogen 7, 12, dimethylbenz[a]anthracene (DMBA) was administered to normal weight and diet-induced obese female Sprague-Dawley rats. Cell proliferation was evaluated by immunohistological staining of BrdU-incorporation. In the mammary glands and inguinal lymphatic nodes of the obese rats, cell proliferation was significantly increased, indicating a significant influence of obesity on breast cancer. Effects of leptin, estrogen, and IGF-I on the proliferation of MCF-7 cells in vitro were assessed using an MTT assay. Cell culture experiments demonstrated a mitogenic role of these three mediators on cell proliferation. Our data demonstrate a stimulative effect of substances produced by the adipose tissue on breast cancer. Body weight specific cell proliferation suggests that obesity-related adipokines and mediators enhance cell proliferation and increase the risk for breast cancer.
KW - Animals
KW - Humans
KW - Female
KW - Immunohistochemistry
KW - Lymphatic Metastasis
KW - Time Factors
KW - Disease Models, Animal
KW - Rats
KW - Rats, Sprague-Dawley
KW - Body Weight
KW - Cell Line, Tumor
KW - Analysis of Variance
KW - Random Allocation
KW - Cell Proliferation
KW - Breast Neoplasms/pathology
KW - Lymph Nodes/metabolism/pathology
KW - 9,10-Dimethyl-1,2-benzanthracene
KW - Adenocarcinoma/pathology
KW - Carcinogens
KW - Dietary Fats/administration & dosage
KW - Estradiol/administration & dosage/metabolism
KW - Groin
KW - Insulin-Like Growth Factor I/administration & dosage/metabolism
KW - Leptin/administration & dosage/metabolism
KW - Mammary Neoplasms, Experimental/chemically induced/pathology
KW - Obesity/metabolism/pathology
KW - Animals
KW - Humans
KW - Female
KW - Immunohistochemistry
KW - Lymphatic Metastasis
KW - Time Factors
KW - Disease Models, Animal
KW - Rats
KW - Rats, Sprague-Dawley
KW - Body Weight
KW - Cell Line, Tumor
KW - Analysis of Variance
KW - Random Allocation
KW - Cell Proliferation
KW - Breast Neoplasms/pathology
KW - Lymph Nodes/metabolism/pathology
KW - 9,10-Dimethyl-1,2-benzanthracene
KW - Adenocarcinoma/pathology
KW - Carcinogens
KW - Dietary Fats/administration & dosage
KW - Estradiol/administration & dosage/metabolism
KW - Groin
KW - Insulin-Like Growth Factor I/administration & dosage/metabolism
KW - Leptin/administration & dosage/metabolism
KW - Mammary Neoplasms, Experimental/chemically induced/pathology
KW - Obesity/metabolism/pathology
M3 - SCORING: Journal article
VL - 61
SP - 484
EP - 491
JO - NUTR CANCER
JF - NUTR CANCER
SN - 0163-5581
IS - 4
M1 - 4
ER -