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Contributor Information

  • Name Anne Lykkesfeldt
  • Institute Danish Cancer Society, Denmark
  • Primary citation Lykkesfeldt et al. 1986. Br J Cancer. 53(1):29-35. PMID: 3947513

Tool Details

  • Tool name: MCF7/TAMR-1 Cell Line
  • Alternate names: MCF-7/TAMR-1; MCF7/TAMR-1; MCF7 TAMR-1; MCF-7/TAM(R)-1; MCF7-TAMR; TAMR-1; TamR-1; TamR1; AL-1
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: MCF7/S0.5 Cell Line
  • Organism: Human
  • Donor: Female; 69 y.o., Caucasian
  • Tissue: Breast
  • Gender: Female
  • Cancer type: Breast cancer
  • Model: Tumour line
  • CRISPR: No
  • Receptors of note: Oestrogen receptor positive and progesterone receptor negative
  • Application: New hormone therapies identification; Elucidating signaling pathways involved in tamoxifen-resistant cancer growth
  • Description: MCF7/TAMR-1 cell line is a stable tamoxifen-resistant subline. This cell line has been established in tissue culture after long term treatment with 1 uM tamoxifen. Tamoxifen (Nolvadex) is a widely used drug for hormone-dependent cancer. Tamoxifen resistance (either primary or acquired) makes oestrogen receptor-positive breast cancer much more difficult to treat.

    This cell line was produced from the parental cell line MCF7/S0.5, as a model cell system to study the effects of tamoxifen resistant cancer growth. MCF7/TAMR-1 cells are oestrogen receptor positive and progesterone receptor negative. They are growth inhibited by the pure antioestrogen fulvestrant.

    Previous applications of this cell line include treatment with steroidal antiestrogens.

    MCF7/TAMR-1 enables identification of new hormone therapies and greater understanding of the signalling pathways/methods behind tamoxifen resistance. Additionally MCF/TAMR-1 can aid in identifying new predictive markers for response to hormonal therapy.
  • Research area: Cancer; Drug development
  • 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 uM 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 uM tamoxifen, which is lethal for the parental MCF7/S0.5 cell line
  • Cellosaurus ID: CVCL_M436
  • Additional notes: During the establishment process the treatment of MCF7/S0.5 cells 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: New hormone therapies identification; Elucidating signaling pathways involved in tamoxifen-resistant cancer growth

Handling

  • Format: Frozen
  • Passage number: 431 (AL3502, AL3503)
  • Growth medium: Phenol red-free DMEM/F-12 containing 1% Fetal bovine serum, 2 mM Glutamax and 6 ng/ml Insulin. To maintain high-level resistance, the medium should be supplemented with 1 uM Tamoxifen
  • Temperature: 37° C
  • Atmosphere: 5% CO2
  • Storage conditions: Liquid Nitrogen
  • Shipping conditions: Dry ice
  • Mycoplasma free: Yes
  • Biosafety level: 1

Documentation

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References

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  • •  Martin et al. 2017. Nat Commun. 8(1):1865. PMID: 29192207
  • •  Guney Eskiler et al. 2016. Cell Biol Toxicol. :. PMID: 27585693
  • •  Joshi et al. 2016. Oncotarget. :. PMID: 27528030
  • •  Leclercq et al. 2016. J Recept Signal Transduct Res. :1-18. PMID: 27400858
  • •  Guest et al. 2016. PLoS One. 11(6):e0157397. PMID: 27308830
  • •  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
  • •  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
  • •  Cutrupi et al. 2012. Oncogene. 31(40):4353-61. PMID: 22249258
  • •  Plaza-Menacho et al. 2010. Oncogene. 29(33):4648-57. PMID: 20531297
  • •  Lykkesfeldt et al. 1994. Cancer Res. 54(6):1587-95. PMID: 8137264
  • •  Lykkesfeldt et al. 1986. Br J Cancer. 53(1):29-35. PMID: 3947513