My focus is on ER+ breast cancer. I am working with MCF-7 cell lines, but need equivalent murine cells to perform immunocompetent implantation assays to track tumor microenvironmental changes. I read 67NR is ER-alpha positive, but would like second opinion regarding it's suitability in my experiments.
Hi Nilesh,
Of course, you are well aware that signaling through growth factor signaling pathways, in particular through receptor tyrosine kinases, has been demonstrated to confer tamoxifen (TF) resistance in an estradiol-independent manner. To that point, as regarding your request on murine breast cancer ER-alpha positive cell line showing sensitivity to TF, please look thru the paper of Susan Waltz et al, published in Neoplasia 12:8, 650-658, 2010. They used to use the R7 cell line, which is a murine mammary epithelial tumor cell line established from a mammary tumor from a transgenic MMTV-Ron mouse. This transgenic mouse model has been described previously. Cell lines were maintained in RPMI, supplemented by 10% fetal bovine serum and 1% penicillin-streptomycin. Transfection of PCI-Neo Ron, PCI-Neo empty vector, ERE-Firefly luciferase, and CMV-Renilla luciferase was carried out using lipofectamine 2000 (Invitrogen).
Ron, like many other receptor tyrosine kinases, is known to signal through the MAPK pathway when activated. Dr. Waltz also revealed the association between activated Ron and phosphorylated MAPK and ER in breast cancer cells. The rescue effect observed with HGFL in the presence of TF is attenuated with inhibition of the MAPK pathway, reinforcing the importance of this mechanism.
Some previously published papers might be of your interest, as well.
CK Osborne, V Bardou, TA Hopp, GC Chamness, SG Hilsenbeck, SA Fuqua, J Wong, DC Allred, GM Clark, R Schiff
Role of the estrogen receptor coactivator AIB1 (SRC-3) and HER-2/neu in tamoxifen resistance in breast cancer
J Natl Cancer Inst, 95 (2003), pp. 353–361
EK Keeton, M Brown
Cell cycle progression stimulated by tamoxifenbound estrogen receptor-a and promoter-specific effects in breast cancer cells deficient in N-CoR and SMRT
Mol Endocrinol, 19 (2005), pp. 1543–1554
J Shou, S Massarweh, CK Osborne, AE Wakeling, S Ali, H Weiss, R Schiff
Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer
J Natl Cancer Inst, 96 (2004), pp. 926–935
H Zhao, F Ou-Yang, IF Chen, MF Hou, SS Yuan, HL Chang, YC Lee, R Plattner, SE Waltz, SM Ho, et al.
Enhanced resistance to tamoxifen by the c-ABL proto-oncogene in breast cancer
Neoplasia, 12 (2010), pp. 214–223
S Kato, H Endoh, Y Masuhiro, T Kitamoto, S Uchiyama, H Sasaki, S Masushige, Y Gotoh, E Nishida, H Kawashima, et al.
Activation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase
Science, 270 (1995), pp. 1491–1494
Best wishes,
Ilya
The short answer is YES. Please check our paper for the details about the cell line in link below.
Link: https://www.ncbi.nlm.nih.gov/pubmed/19890043
Yes, According to Anderson et al, 67NR expresses ERalfa and responds to Tamoxifen.
Article Functional and molecular characterisation of EO771.LMB, a ne...
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