MCF7/S0.5 Cell Line
Invented by Dr Anne Lykkesfeldt at Danish Cancer Society
Catalogue Number | 152087 |
Antigen/Gene or Protein Targets | Oestrogen receptor |
Parental Line | MCF7 S0.5 |
Host | Human |
Tissue | Breast |
Disease Keywords | Breast cancer, tamoxifen-resistant |
Model | Tumour line |
Relevance | The MCF7/TAMR-7 Cell line is a breast cancer cell line resistant to tamoxifen.Tamoxifen is by far the most widely used drug for hormone-dependent breast cancer. However, primary or acquired resistance to Tamoxifen severely limits its clinical effectiveness. The MCF7/TAMR-7 cell line is a good model cell to study the signalling pathways, which are the major drivers of tamoxifen-resistant growth. |
Production Details | The parental cell line for the MCF7/TAMR-7 cells is MCF7/S0.5, which was adapted to grow at low serum concentration in order to study the effect of estradiol and tamoxifen. MCF7/TAMR-7 has been established from a clone of cells that survived long term treatment with 1 µM tamoxifen. Tamoxifen-resistant cells are passaged continuously in presence of 1 µM tamoxifen, which is lethal for the parental MCF7/S0.5 cell line. |
Research Area | Cancer, Drug Discovery & Development |
Recommended Growing Conditions | 37°C under 5% CO2 in air using phenol red-free DMEM:Ham’s F-12 containing 1% fetal bovine serum, 2 mM Glutamax and 6 ng/ml insulin. To maintain high-level resistance, medium was supplemented with Tamoxifen (1 μM). |
Positive Control | MCF7-S0.5 (parental cell line) |
Notes |
MCF7/TAMR-7 cells are oestrogen receptor positive and progesterone receptor negative. MCF7/TAMR-7 cells are growth inhibited by the pure antioestrogen fulvestrant. The oestrogen receptor is a major driver of growth of MCF7/TAMR-7 cell. The TAMR lines were established from the MCF7/S0.5 cell line, which was adapted to grow with 0.5% fetal calf serum in phenol red containing DMEM/F12 medium. Treatment with tamoxifen was started in passage 351. Few colonies of cells survived the treatment and after 28 days of tamoxifen treatment, tamoxifen was omitted from the medium for 22 days. After 19 passages without tamoxifen (passage 372) the cells underwent a second treatment with tamoxifen which initially reduced cell growth rate, but around 390-400 the growth rate of the tamoxifen resistant cell lines was close to the growth rate of the parental MCF7/S0.5 cells. |
Cellosaurus ID | 1D43 |
Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.
Elias et al. 2015. Oncogene. 34(15):1919-27. PMID: 24882577.
New cell culture model for aromatase inhibitor-resistant breast cancer shows sensitivity to fulvestrant treatment and cross-resistance between letrozole and exemestane.
Europe PMC ID: 25625755
Pedersen et al. 2014. Int J Oncol. 45(5):2167-75. PMID: 25175082.
Sorafenib and nilotinib resensitize tamoxifen resistant breast cancer cells to tamoxifen treatment via estrogen receptor α.
Europe PMC ID: 25175082
Lundqvist et al. 2014. Steroids. 85:30-5. PMID: 24747771.
Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy.
Europe PMC ID: 24882577
1α,25-dihydroxyvitamin D3 inhibits cell growth and NFκB signaling in tamoxifen-resistant breast cancer cells.
Europe PMC ID: 24747771
Thrane et al. 2013. Breast Cancer Res Treat. 139(1):71-80. PMID: 23609470.
Estrogen receptor α is the major driving factor for growth in tamoxifen-resistant breast cancer and supported by HER/ERK signaling.
Europe PMC ID: 23609470
Larsen et al. 2012. Int J Oncol. 41(5):1863-70. PMID: 22961366.
Carboplatin treatment of antiestrogen-resistant breast cancer cells.
Europe PMC ID: 22961366
Frankel et al. 2007. Breast Cancer Res Treat. 104(2):165-79. PMID: 17061041.
Protein Kinase C alpha is a marker for antiestrogen resistance and is involved in the growth of tamoxifen resistant human breast cancer cells.
Europe PMC ID: 17061041
Berstein et al. 2003. Endocr Relat Cancer. 10(2):267-77. PMID: 12790788.
New approaches to the understanding of tamoxifen action and resistance.
Europe PMC ID: 12790788
Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.
Elias et al. 2015. Oncogene. 34(15):1919-27. PMID: 24882577.
New cell culture model for aromatase inhibitor-resistant breast cancer shows sensitivity to fulvestrant treatment and cross-resistance between letrozole and exemestane.
Pedersen et al. 2014. Int J Oncol. 45(5):2167-75. PMID: 25175082.
Sorafenib and nilotinib resensitize tamoxifen resistant breast cancer cells to tamoxifen treatment via estrogen receptor α.
Lundqvist et al. 2014. Steroids. 85:30-5. PMID: 24747771.
Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy.
1α,25-dihydroxyvitamin D3 inhibits cell growth and NFκB signaling in tamoxifen-resistant breast cancer cells.
Thrane et al. 2013. Breast Cancer Res Treat. 139(1):71-80. PMID: 23609470.
Estrogen receptor α is the major driving factor for growth in tamoxifen-resistant breast cancer and supported by HER/ERK signaling.
Larsen et al. 2012. Int J Oncol. 41(5):1863-70. PMID: 22961366.
Carboplatin treatment of antiestrogen-resistant breast cancer cells.
Frankel et al. 2007. Breast Cancer Res Treat. 104(2):165-79. PMID: 17061041.
Protein Kinase C alpha is a marker for antiestrogen resistance and is involved in the growth of tamoxifen resistant human breast cancer cells.
Berstein et al. 2003. Endocr Relat Cancer. 10(2):267-77. PMID: 12790788.
New approaches to the understanding of tamoxifen action and resistance.