Journal
BREAST CANCER RESEARCH AND TREATMENT
Volume 79, Issue 1, Pages 95-105Publisher
KLUWER ACADEMIC PUBL
DOI: 10.1023/A:1023326121951
Keywords
human breast cancer; human breast epithelial cells; MCF10A; NNK; tobacco-specific carcinogen; tumor
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Funding
- NCI NIH HHS [1R29CA69530] Funding Source: Medline
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Repeated treatments of non-cancerous human breast epithelial cells MCF10A with a low dose of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) induced the development of cancerous cells. NNK-transformed MCF10A cells acquired cancerous properties including anchorage-independent cell growth and increased cell motility. Cellular transformation of MCF10A cells was accompanied by a loss of responsiveness to 17beta-estradiol and decreased rate of cell proliferation. NNK-transformed MCF10A cells were also tumorigenic in immunodifficient mice. Studies of changes in the regulation of intracellular signaling pathways revealed that the upstream Erk pathway was down-regulated in the NNK-transformed cells. Our data provide the first evidence suggesting that the tobacco carcinogen NNK is competent to induce malignant transformation of noncancerous human breast epithelial cells. Our findings suggest that the tobacco carcinogen NNK may contribute to early events in human breast carcinogenesis.
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