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, Vol. 61, No. 4, 4, 2009, p. 484-491.

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@article{d485937f78a4483f8ad667128792e786,
title = "Obesity and the associated mediators leptin, estrogen and IGF-I enhance the cell proliferation and early tumorigenesis of breast cancer cells.",
abstract = "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.",
keywords = "Animals, Humans, Female, Immunohistochemistry, Lymphatic Metastasis, Time Factors, Disease Models, Animal, Rats, Rats, Sprague-Dawley, Body Weight, Cell Line, Tumor, Analysis of Variance, Random Allocation, *Cell Proliferation, Breast Neoplasms/pathology, Lymph Nodes/metabolism/pathology, 9,10-Dimethyl-1,2-benzanthracene, Adenocarcinoma/pathology, Carcinogens, Dietary Fats/administration & dosage, Estradiol/administration & dosage/*metabolism, Groin, Insulin-Like Growth Factor I/administration & dosage/*metabolism, Leptin/administration & dosage/*metabolism, Mammary Neoplasms, Experimental/chemically induced/*pathology, Obesity/metabolism/*pathology, Animals, Humans, Female, Immunohistochemistry, Lymphatic Metastasis, Time Factors, Disease Models, Animal, Rats, Rats, Sprague-Dawley, Body Weight, Cell Line, Tumor, Analysis of Variance, Random Allocation, *Cell Proliferation, Breast Neoplasms/pathology, Lymph Nodes/metabolism/pathology, 9,10-Dimethyl-1,2-benzanthracene, Adenocarcinoma/pathology, Carcinogens, Dietary Fats/administration & dosage, Estradiol/administration & dosage/*metabolism, Groin, Insulin-Like Growth Factor I/administration & dosage/*metabolism, Leptin/administration & dosage/*metabolism, Mammary Neoplasms, Experimental/chemically induced/*pathology, Obesity/metabolism/*pathology",
author = "Anne Lautenbach and Anne Budde and Wrann, {Christiane D} and Birgit Teichmann and Gertrud Vieten and Tim Karl and Heike Nave",
year = "2009",
language = "English",
volume = "61",
pages = "484--491",
journal = "NUTR CANCER",
issn = "0163-5581",
publisher = "Routledge",
number = "4",

}

RIS

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 -