Abstract
Results Let-R cells have higher levels of ERa compared to Aros. CyclinD1 basal levels are elevated in Aro cells compared to Let-Rs. Levels of JNK and c-jun are higher in Let-R cells compared to Aros. A highly effective ERa knockdown in Let-R cells was optimized. Conclusions The significant ERa knockdown achieved in the Let-R cells will enable further examination of knockdown effects on protein levels and mRNA expression. Elevated expression of ERa in the Let-R cells observed is consistent with the association between AI resistance and ER hypersensitivity. In resistant cells, the decrease in basal levels of CyclinD1 may be partly responsible for the lack of regulation of classical genes like pS2, previously detected by the lab. The elevated levels of JNK and c-jun observed in Let-R cells supports the theory of crosstalk between the ER and growth factor pathways in resistance. Furthermore, it would be of interest to accompany AI treatments with growth factor inhibitors to further our understanding of endocrine resistance.
Highlights
Aromatase inhibitors (AI) are a novel adjuvant endocrine treatment for estrogen receptor (ER)-positive, postmenopausal breast cancer
This study aims to characterise the Let-R cell line created in the lab and to optimise an ERa knockdown in Let-R cells
The significant ERa knockdown achieved in the Let-R cells will enable further examination of knockdown effects on protein levels and mRNA expression
Summary
Aromatase inhibitors (AI) are a novel adjuvant endocrine treatment for estrogen receptor (ER)-positive, postmenopausal breast cancer. Characterising an aromatase inhibitor resistant breast cancer cell line From International Conference for Healthcare and Medical Students 2011 Dublin, Ireland. Introduction Aromatase inhibitors (AI) are a novel adjuvant endocrine treatment for estrogen receptor (ER)-positive, postmenopausal breast cancer.
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