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Tamoxifen affects PLCg1 expression in ER+ breast cancer cells
Author(s) -
Vergne Ralphdy,
Ortiz Carmen,
Godoy Lenin,
Matta Jaime
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.936.2
Subject(s) - tamoxifen , mcf 7 , cancer research , breast cancer , cell growth , cell culture , estrogen receptor , cell , medicine , cancer , biology , oncology , genetics , human breast
Phospholipase C gamma 1 (PLCg1) can be found in the cytoplasm and in the nucleus of the cells and is involved in signal transduction pathways and proliferation. Previous data from our lab shows that PLCg1 expression in breast cancer cells is higher in comparison to non‐tumorigenic cells. Also, oxidative stress‐induced PLCg1 activation enhances cell survival. Many anticancer drugs can cause oxidative stress as a side effect, such as tamoxifen. Tamoxifen is currently used for the treatment of both early and advanced estrogen receptor positive (ER+) breast cancer in pre‐ and post‐menopausal women. In addition, patients using tamoxifen have a higher probability to develop oxidative stress by consequence of the drug. Our aim is to compare and analyze PLCg1 expression in an ER+ breast cancer cell line (MCF‐7) under the effect of tamoxifen. Our hypothesis is that there will be a high expression of PLCg1 in cells treated with tamoxifen in comparison to untreated cells. To achieve this, we cultured MCF‐7 cells using complete media without phenol red and 4μM tamoxifen. After 24hrs, cells were lysed and protein and RNA were extracted. To determine PLCg1 expression we used a Taqman gene expression assay using GAPDH as housekeeping gene. Our results shows that PLCg1 expression was two times higher in MCF‐7 cells treated with tamoxifen compared to untreated cells at 24 hrs. However, this effect was not statistically significant. This preliminary data indicates that the PLCg1 expression might be involved in ER modulation. Currently, we are developing an MCF‐7 cell line resistant to tamoxifen to further study the changes in PLCg1 protein and gene expression upon acquired resistance. Support or Funding Information This work was supported by the UPR‐PRISE Program Grant #R25GM096955 and NIGMS‐NIH grants R25GM082406 (CO), and 9SC1CA182846‐04. We also acknowledge the support of the Molecular and Genomics Core at Ponce Health Sciences University (NIMHD Grant MD007579).