T47D human breast cancer cells were cultured in estrogen-deficient media for up to 32 months and the resulting cell line (L(hE(-))) exhibited unique phenotypic and genotypic characteristics. Compared to low passage (L) cells, the L(hE(-)) cells exhibited a significantly higher rate of proliferation,
Interaction of growth factors during progression towards steroid independence in T-47-D human breast cancer cells
β Scribed by Roger J. Daly; Roger J. B. King; Philippa D. Darbre
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 874 KB
- Volume
- 43
- Category
- Article
- ISSN
- 0730-2312
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β¦ Synopsis
When deprived of steroid in the long term, T-47-D human breast cancer cells lose estrogen sensitivity of cell growth. This loss of response results from an increased basal growth rate in the absence of steroid, not from a loss of estrogen-stimulated growth, and it occurs without any loss of estrogen receptor number or function. Growth factor gene expression and sensitivity have been investigated in this model system in an attempt to unravel the molecular mechanisms underlying the progression to steroid autonomy. The transition was accompanied by a decreased dependence on added serum and by a loss of the stimulatory effects of insulin and basic fibroblast growth factor, but also by an acquired sensitivity to stimulation by transforming growth factor-p (TGF-p). An increase in TGF-6, mRNA was detected following loss of steroid sensitivity. There was no increase in epidermal growth factor (EGF) receptor number. These findings are discussed in relation to current knowledge concerning the mechanisms by which estrogens stimulate breast cancer cell proliferation.
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