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Cell Lines

T47D/TR-2 Cell Line

Invented by Dr Anne Lykkesfeldt from Danish Cancer Society
Invented at Danish Cancer Society
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Adapted Larsen et al. 2015. PLoS One. 10(2):e0118346. PMID: 25706943 Fig. Effect of dasatinib on expression of Src and downstream signaling in parental and resistant cells and identification of Src dimers. (A) Western blot showing expression of total and phosphorylated Src (Tyr416) in lysates from parental (T47D/S2 and T47D/S5), tamoxifen (TR-1 and TR-2) and fulvestrant (182R-1 and 182R-2) resistant cell lines grown under their standard conditions. β-actin was used as loading control. (B) Western blot showing expression of total and phosphorylated Akt (Ser473), Erk (Thr202/Tyr204) and Src (Tyr416) in lysates from parental (T47D/S2 and T47D/S5), tamoxifen (TR-1 and TR-2) and fulvestrant (182R-1 and 182R-2) resistant cell lines grown with or without dasatinib (1 μM) for 1 hour. Hsp70 was used as loading control. (C) Src dimers in parental (T47D/S2 and T47D/S5), tamoxifen (TR-1 and TR-2) and fulvestrant (182R-1 and 182R-2) resistant cell lines grown under their standard conditions. Src protein was immunoprecipitated from 1 mg total protein lysates. Western analysis for HER receptors, Src and ER was performed on both total protein lysates and immunoprecipitated samples. A representative experiment out of two is shown. β-actin was used as loading control.
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Catalogue Number 152110
Antigen/Gene or Protein Targets Oestrogen receptor
Parental Line T47D/S2
Host Human
Tissue Breast
Disease Keywords Breast carcinoma, tamoxifen-resistant
Model Tumour line
Relevance The T47D/TR-2 Cell line is a breast cancer cell line resistant to tamoxifen. Antiestrogen resistance is a major problem in breast cancer treatment. Therefore, the search for new therapeutic targets and biomarkers for antiestrogen resistance is crucial. This cell line allows the study of the mechanisms involved in tamoxifen resistant breast cancer cell growth.
Production Details The T47D/TR-2 cell line has been established by long term treatment of T47D/S2 cells with 1 µM tamoxifen. Clonal selection was performed in medium without tamoxifen. After growth in presence of 1 µM tamoxifen for 10 months, the growth rate was similar to the parental cells.
Research Area Cancer, Drug Discovery & Development
Recommended Growing Conditions Phenol red free RPMI 1640 + 2% FCS + glutamax + 8µg Insulin/ml + 1 uM tamoxifen
Notes T47D/TR-2 cells are ER alpha positive and express progesterone receptor, although at reduced level compared to parental T7D/S2 cells. T47D/TR-2 are growth inhibited by fulvestrant.

Passage 164 (AL3575, AL3576)
Cellosaurus ID CVCL_1D37

References

There are 6 reference entries for this reagent.

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References: 6 entries

Larsen et al. 2015. PLoS One. 10(2):e0118346. PMID: 25706943.

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Larsen et al. 2015. BMC Cancer. 15:239. PMID: 25885472.

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Aurora kinase B is important for antiestrogen resistant cell growth and a potential biomarker for tamoxifen resistant breast cancer.

Europe PMC ID: 25885472

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SRC drives growth of antiestrogen resistant breast cancer cell lines and is a marker for reduced benefit of tamoxifen treatment.

Europe PMC ID: 25706943

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Thrane et al. 2014. Oncogene. :. PMID: 25362855.

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A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.

Europe PMC ID: 25362855

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References: 6 entries

Larsen et al. 2015. PLoS One. 10(2):e0118346. PMID: 25706943.

View  

Larsen et al. 2015. BMC Cancer. 15:239. PMID: 25885472.

View  

Aurora kinase B is important for antiestrogen resistant cell growth and a potential biomarker for tamoxifen resistant breast cancer.

View  

SRC drives growth of antiestrogen resistant breast cancer cell lines and is a marker for reduced benefit of tamoxifen treatment.

View  

Thrane et al. 2014. Oncogene. :. PMID: 25362855.

View  

A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.

View  

Add a reference

Inventor Information