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Contributor Information

  • Name Anne Lykkesfeldt
  • Institute Danish Cancer Society

Tool Details

  • Tool name: MCF7/TAMR-4 Cell Line
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: MCF7 S0.5
  • Organism: Human
  • Tissue: Breast
  • Cancer type: Breast; Tamoxifen resistant
  • Disease: Cancer
  • Model: Tumour line
  • Conditional: Yes
  • Description: The MCF7/TAMR-4 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-4 cell line is a good model cell to study the signalling pathways which are the major drivers of tamoxifen-resistant growth.
  • Research area: Cancer; Drug Discovery & Development
  • Production details: The parental cell line for the MCF7/TAMR-4 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-4 has been established from a clone of cells that survived long term treatment with 1 ÂľM tamoxifen. Tamoxifen-resistant cells are passaged continuously in presence of 1 ÂľM tamoxifen, which is lethal for the parental MCF7/S0.5 cell line.
  • Cellosaurus ID: CVCL_1D42
  • Additional notes: MCF7/TAMR-4 cells are oestrogen receptor positive and progesterone receptor negative. MCF7/TAMR-4 cells are growth inhibited by the pure antiestrogen fulvestrant. The oestrogen receptor is a major driver of growth of MCF7/TAMR-4 cell, ref 1. 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.

  • For Research Use Only

Target Details

  • Target: Oestrogen receptor

Application Details

  • Application notes: MCF7/TAMR-4 cells are oestrogen receptor positive and progesterone receptor negative. MCF7/TAMR-4 cells are growth inhibited by the pure antiestrogen fulvestrant. The oestrogen receptor is a major driver of growth of MCF7/TAMR-4 cell, ref 1. 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 402 (AL3482), 403 (AL2753)

Handling

  • Format: Frozen
  • Passage number: Passage 402 (AL3482), 403 (AL2753)
  • Growth medium: 37°C under 5% CO2 in air using phenol red-free DMEM:Ham’s F-12 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 ?M).
  • Storage conditions: Liquid Nitrogen
  • Shipping conditions: Dry ice
  • Mycoplasma free: Yes
  • Biosafety level: 1

Documentation

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  • Available on request

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References

  • •  Joshi et al. 2016. Oncotarget. :. PMID: 27528030.
  • •  Integrative analysis of miRNA and gene expression reveals regulatory networks in tamoxifen-resistant breast cancer.
  • •  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.
  • •  Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy.
  • •  Thrane et al. 2013. Breast Cancer Res Treat. 139(1):71-80. PMID: 23609470.
  • •  Estrogen receptor a 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.
  • •  Millour et al. 2010. Oncogene. 29(20):2983-95. PMID: 20208560.
  • •  FOXM1 is a transcriptional target of ERalpha and has a critical role in breast cancer endocrine sensitivity and resistance.
  • •  Pancholi et al. 2008. Endocr Relat Cancer. 15(4):985-1002. PMID: 18824559.
  • •  ERBB2 influences the subcellular localization of the estrogen receptor in tamoxifen-resistant MCF-7 cells leading to the activation of AKT and RPS6KA2.
  • •  Sarwar et al. 2006. Endocr Relat Cancer. 13(3):851-61. PMID: 16954434.
  • •  Phosphorylation of ERalpha at serine 118 in primary breast cancer and in tamoxifen-resistant tumours is indicative of a complex role for ERalpha phosphorylation in breast cancer progression.