MCF7/S0.5 Cell Line
Invented by Dr Anne Lykkesfeldt at Danish Cancer Society
MCF7/TAMR-1 Human Breast Cancer Cell Line
Invented by Dr Anne Lykkesfeldt from Danish Cancer Society
Invented at Danish Cancer Society
- Datasheet
- References (29)
- Inventor Info
Info
| Catalogue Number | 152089 |
| 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 |
Tamoxifen resistant cell line which can be used to discover alternative treatments for breast cancer and understand the signalling pathways involved in tamoxifen resistance. Background and Research Application The MCF7/TAMR-1 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-1 cell line is a good model cell, to study the signalling pathways, which are the major drivers of tamoxifen-resistant growth. This cell line was produced as an adaptation of an original cell line (MCF7/S0.5), as a model cell system to study the effects of tamoxifen resistant cancer growth. This enables, identification of new hormone therapies and greater understanding of the signalling pathways/methods behind tamoxifen resistance. |
| Production Details | The parental cell line for the MCF7/TAMR-1 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-1 has been established from a clone of cells that survived long term treatment with 1 µM tamoxifen. The establishment of the MCF7/TAMR-1 cell line, originally named AL-1, was first described in Lykkesfeldt et al (1986). 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 |
Points of Interest Estrogen receptor-positive breast cancer is the most common form of breast cancer, with approximately 80% of all breast cancers expressing the estrogen receptor (ER). They depend on the estrogen hormone to facilitate the growth and expansion of cancer cells. Hormone therapy (e.g. tamoxifen) can limit the growth of ER breast cancers by blocking the actions of estrogen. Tamoxifen resistance (either primary or acquired) makes ER+ breast cancer much more difficult to treat. MCF7/TAMR-1 cell line is able to survive with tamoxifen in growth medium, allowing the resistance to be understood and prospective new treatment options to be discovered. MCF7/TAMR-1 cells are oestrogen receptor positive and progesterone receptor negative. MCF7/TAMR-1 cells are growth inhibited by the pure antioestrogen fulvestrant. The oestrogen receptor is a major driver of growth of MCF7/TAMR-1 cell. Treatment targeting the Aurora kinase A restores sensitivity to tamoxifen treatment. 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. Passage 431 (AL3502, AL3503) Concentration Vial has between 1-5 million cells as standard, however this may vary. |
| Cellosaurus ID | CVCL_M436 |
References: 29 entries
Lee et al. 2018. Autophagy. 14(5):812-824. PMID: 29130361.
Martin et al. 2017. Nat Commun. 8(1):1865. PMID: 29192207.
An in vitro model for the development of acquired tamoxifen resistance.
Europe PMC ID: 27585693
Guney Eskiler et al. 2016. Cell Biol Toxicol. :. PMID: 27585693.
Joshi et al. 2016. Oncotarget. :. PMID: 27528030.
Integrative analysis of miRNA and gene expression reveals regulatory networks in tamoxifen-resistant breast cancer.
Europe PMC ID: 27528030
ERα dimerization: a key factor for the weak estrogenic activity of an ERα modulator unable to compete with estradiol in binding assays.
Europe PMC ID: 27400858
Leclercq et al. 2016. J Recept Signal Transduct Res. :1-18. PMID: 27400858.
Guest et al. 2016. PLoS One. 11(6):e0157397. PMID: 27308830.
Src Is a Potential Therapeutic Target in Endocrine-Resistant Breast Cancer Exhibiting Low Estrogen Receptor-Mediated Transactivation.
Europe PMC ID: 27308830
High CDK6 Protects Cells from Fulvestrant-Mediated Apoptosis and is a Predictor of Resistance to Fulvestrant in Estrogen Receptor-Positive Metastatic Breast Cancer.
Europe PMC ID: 27252418
Alves et al. 2016. Clin Cancer Res. :. PMID: 27252418.
Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.
Elias et al. 2015. Oncogene. 34(15):1919-27. PMID: 24882577.
Thrane et al. 2014. Oncogene. PMID: 25362855.
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
Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
Europe PMC ID: 24983248
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
Nass et al. 2014. PLoS One. 9(7):e101473. PMID: 24983248.
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
Cutrupi et al. 2012. Oncogene. 31(40):4353-61. PMID: 22249258.
Targeting of the adaptor protein Tab2 as a novel approach to revert tamoxifen resistance in breast cancer cells.
Europe PMC ID: 22249258
Plaza-Menacho et al. 2010. Oncogene. 29(33):4648-57. PMID: 20531297.
Targeting the receptor tyrosine kinase RET sensitizes breast cancer cells to tamoxifen treatment and reveals a role for RET in endocrine resistance.
Europe PMC ID: 20531297
Lykkesfeldt et al. 1994. Cancer Res. 54(6):1587-95. PMID: 8137264.
Altered expression of estrogen-regulated genes in a tamoxifen-resistant and ICI 164,384 and ICI 182,780 sensitive human breast cancer cell line, MCF-7/TAMR-1.
Europe PMC ID: 8137264
Lykkesfeldt et al. 1986. Br J Cancer. 53(1):29-35. PMID: 3947513.
Indirect mechanism of oestradiol stimulation of cell proliferation of human breast cancer cell lines.
Europe PMC ID: 3947513
Add a reference
References: 29 entries
Lee et al. 2018. Autophagy. 14(5):812-824. PMID: 29130361.
Martin et al. 2017. Nat Commun. 8(1):1865. PMID: 29192207.
An in vitro model for the development of acquired tamoxifen resistance.
Guney Eskiler et al. 2016. Cell Biol Toxicol. :. PMID: 27585693.
Joshi et al. 2016. Oncotarget. :. PMID: 27528030.
Integrative analysis of miRNA and gene expression reveals regulatory networks in tamoxifen-resistant breast cancer.
ERα dimerization: a key factor for the weak estrogenic activity of an ERα modulator unable to compete with estradiol in binding assays.
Leclercq et al. 2016. J Recept Signal Transduct Res. :1-18. PMID: 27400858.
Guest et al. 2016. PLoS One. 11(6):e0157397. PMID: 27308830.
Src Is a Potential Therapeutic Target in Endocrine-Resistant Breast Cancer Exhibiting Low Estrogen Receptor-Mediated Transactivation.
High CDK6 Protects Cells from Fulvestrant-Mediated Apoptosis and is a Predictor of Resistance to Fulvestrant in Estrogen Receptor-Positive Metastatic Breast Cancer.
Alves et al. 2016. Clin Cancer Res. :. PMID: 27252418.
Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.
Elias et al. 2015. Oncogene. 34(15):1919-27. PMID: 24882577.
Thrane et al. 2014. Oncogene. PMID: 25362855.
A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.
Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy.
Nass et al. 2014. PLoS One. 9(7):e101473. PMID: 24983248.
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.
Cutrupi et al. 2012. Oncogene. 31(40):4353-61. PMID: 22249258.
Targeting of the adaptor protein Tab2 as a novel approach to revert tamoxifen resistance in breast cancer cells.
Plaza-Menacho et al. 2010. Oncogene. 29(33):4648-57. PMID: 20531297.
Targeting the receptor tyrosine kinase RET sensitizes breast cancer cells to tamoxifen treatment and reveals a role for RET in endocrine resistance.
Lykkesfeldt et al. 1994. Cancer Res. 54(6):1587-95. PMID: 8137264.
Altered expression of estrogen-regulated genes in a tamoxifen-resistant and ICI 164,384 and ICI 182,780 sensitive human breast cancer cell line, MCF-7/TAMR-1.
Lykkesfeldt et al. 1986. Br J Cancer. 53(1):29-35. PMID: 3947513.
Indirect mechanism of oestradiol stimulation of cell proliferation of human breast cancer cell lines.
Add a reference
