#152555

MCF7/ExeR-1 Cell Line

Cat. #152555

MCF7/ExeR-1 Cell Line

Cat. #: 152555

Sub-type: Continuous

Unit size: 1x10^6 cells / vial

Organism: Human

Tissue: Breast

Disease: Cancer

£800.00

This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.

Contributor

Inventor: Anne Lykkesfeldt

Institute: Danish Cancer Society, Denmark

Primary Citation: Hole et al. 2015. Int J Oncol. 46(4):1481-1490. PMID: 25625755.

Tool Details
Target Details
Applications
Handling
Related Tools
References

Tool Details

*FOR RESEARCH USE ONLY

  • Name: MCF7/ExeR-1 Cell Line
  • Alternate name: MCF-7/ExeR-1; ExeR-1
  • Tool sub type: Continuous
  • Parental cell: MCF7
  • Organism: Human
  • Gender: Female
  • Tissue: Breast
  • Disease: Cancer
  • Growth properties: Breast cancer cell line resistant to the aromatase inhibitor exemestane. Estrogen receptor positive. Progesterone receptor positive when grown in medium without exemestane.
  • Conditional: No
  • Description: MCF7/ExeR-1 is a cell culture model mimicking acquired resistance of aromatase inhibitors (AIs) - an anti-cancer therapy. This breast cancer cell line was established from MCF7 cells. The cellular classification is epithelial, and their shape is polygonal.The MCF7/ExeR-1 cell line is resistant to the third generation AI - exemestane (Aromasin). Third generation AIs have proven to be effective treatment for oestrogen receptor positive (ER+) breast cancer and as such are recommended as first line endocrine therapy for postmenopausal ER+ breast cancer patients. However, a major problem is development of resistance against AIs. Previous applications of this cell line include western blot analysis of protein expression. Since molecular mechanisms of AI resistance are largely undisclosed, the development of cell lines resistant to the non-steroidal AI exemestane allows the study of the molecular basis for AI resistance to find new targets for treatment.
  • Application: Investigation of molecular mechanisms of exemestane resistance
  • Production details: Exemestane-resistant cell lines were established from MCF-7 cells grown in medium with 10% NCS and 10-7 M testosterone. A culture of MCF-7 cells were treated with 10-7 M exemestane for one week, trypsinised and seeded in serial dilutions in 24-well plates. Single colonies were transferred to new wells and gradually expanded in medium with exemestane. After ~2-3 months, the isolated colonies gave rise to exemestane-resistant cell lines, which could be grown in exemestane-containing medium with...
  • Cellosaurus id: CVCL_5A13

Target Details

  • Target: Exemestane resistance

Applications

  • Application: Investigation of molecular mechanisms of exemestane resistance
  • Application notes: Human breast cancer cell line derived from MCF-7 cells Other related cell lines: - LetR-1, LetR-2, LetR-3 and LetR-4 resistant to the non-steroidal AI letrozole - ExeR-2, ExeR-3 and ExeR-4 resistant to the steroidal AI exemestane - AnaR-1, AnaR-2, AnaR-3 and AnaR-4 resistant to the non-steroidal AI anastrozole Passage 430 (AL3058, AL3059)

Handling

  • Format: Frozen
  • Passage number: Passage 430 (AL3058, AL3059)
  • Growth medium: Phenol-red-free DMEM/F12 medium supplemented with 10% newborn calf serum, 2.5 mM Glutamax, 6 ng/ ml insulin, 0.1 uM testosterone and 0.1 uM exemestane.
  • Temperature: 37° C
  • Atmosphere: Humidified air with 5% CO2
  • Unit size: 1x10^6 cells / vial
  • Shipping conditions: Dry ice

Related Tools

  • Related tools: MCF7/ExeR-2 Cell Line ; MCF7/ExeR-3 Cell Line ; MCF7/ExeR-4 Cell Line Other related cell lines: - LetR-1, LetR-2, LetR-3 and LetR-4 resistant to the non-steroidal AI letrozole - ExeR-2, ExeR-3 and ExeR-4 resistant to the steroidal AI exemestane - AnaR-1, AnaR-2, AnaR-3 and AnaR-4 resistant to the non-steroidal AI anastrozole

References

  • Hole et al. 2015. Breast Cancer Res Treat. 149(3):715-726. PMID: 25667100.
  • Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.