Establishment and characterization of a cell line of human breast carcinoma origin

Keydar, Iafa; Chen, L.; Karby, Shulamit; Weiss, Friedbert; Delarea, Jacob; Radu, Maria; S, Chaitcik; Brenner, H.

doi:10.1016/0014-2964(79)90139-7

Cited by 565 publications

(269 citation statements)

References 12 publications

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“…The human PR exists in two isoforms, a B isoform (PR-B) and an N-terminal truncated A isoform (PR-A), possessing different transcriptional capacities, despite similar hormone-and DNA-binding properties (Kastner et al, 1990;Sartorius et al, 1994;Wen et al, 1994;Richer et al, 2002). T47D cells, here referred to as T47D-WT cells, express both PR-A and -B in an oestrogendependent manner (Keydar et al, 1979;Sutherland et al, 1992). T47D-CO cells express both isoforms of PR independent of ER-a function (Horwitz et al, 1982).…”

Section: Resultsmentioning

confidence: 99%

Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells

et al. 2006

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Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The aIR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IRstimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness.

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Section: Resultsmentioning

confidence: 99%

Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells

et al. 2006

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“…T47D clone 11 human breast cancer cells were obtained from the pleural effusion of infiltrating duct carcinoma [11] and were a gift from Prof. I. Keydar (Tel-Aviv University).…”

Section: Methodsmentioning

confidence: 99%

NMR studies of the lipid metabolism of T47D human breast cancer spheroids

1990

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The in vivo 31p NMR spectrum of T47D human breast cancer cells grown as spheroids shows changes in the phosphomonoester lipid precursors as a function of spheroid size. The ratio of phosphorylethanolamine (PE) to phosphorylcholine (PC) was 1.0_ 0.3 for 3-day-old, 150 tan spheroids. This ratio increased to 2.4+0.4 for spheroids 7 days and older and which were at least 300/tm in diameter. To investigate the phosphatidylethanolamine to phosphatidylcholine (PdylE/PdylC) ratio in the membranes, chloroform/methanol extracts of spheroids were performed. The 31p spectrum of these extracts showed no change with spheroid size, namely the PdylE/PdylC ratio was 0.55-0.06 for spheroids of all ages suggesting that membrane composition is strongly regulated at the precursor level.Nuclear magnetic resonance; T47D; Breast cancer; Lipid metabolism; Phosphomonoester; Spheroid

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“…Cell lines 184 (Stampfer and Bartley, 1985) and 184B5 (Walen and Stampfer, 1989) were derived from non malignant breast epithelial cells; BT-483 (Lasfargues et al, 1978), MCF-7M (Soule et al, 1973), MDA ± MB-134 (Cailleau et al, 1974), MDA ± MB-361 (Cailleau et al, 1978) and T-47D (Keydar et al, 1979) cell lines originated from estrogen receptor (ER) positive breast cancer cells; BT-20 (Lasfargues and Ozzello, 1958), BT-549 (Lasfargues et al, 1978), MDA ± MB-231 (Cailleau et al, 1974), SK-BR-3 (Trempe and Fogh, 1973) cell lines originated from ER negative breast cancer cells. The HBL-100 cell line is an ER negative transformed cell line, originating from normal lactating breast (Caron de Fromentel et al, 1985).…”

Section: Breast Cell Linesmentioning

confidence: 99%

Expression and function of members of the cytokine receptor superfamily on breast cancer cells

et al. 1997

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Establishment and characterization of a cell line of human breast carcinoma origin

Cited by 565 publications

References 12 publications

Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells

Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells

NMR studies of the lipid metabolism of T47D human breast cancer spheroids

Expression and function of members of the cytokine receptor superfamily on breast cancer cells

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