Moonlighting Proteins and Cardiopathy in the Spatial Response of MCF‐7 Breast Cancer Cells to Tamoxifen
Background: The purpose of this study is to apply quantitative high‐throughput proteomics methods to investigate dynamic aspects of protein changes in nucleocytoplasmic distribution of proteins and of total protein abundance for MCF‐7 cells exposed to tamoxifen (Tam) in order to reveal the agonistic and antagonistic roles of the drug. Experimental design: The MS‐based global quantitative proteomics with the analysis of fractions enriched in target subcellular locations is applied to measure the changes in total abundance and in the compartmental abundance/distribution between the nucleus and cytoplasm for several thousand proteins differentially expressed in MCF‐7 cells in response to Tam stimulation. Results: The response of MCF‐7 cells to the Tam treatment shows significant changes in subcellular abundance rather than in their total abundance. The bioinformatics study reveals the relevance of moonlighting proteins and numerous pathways involved in Tam response of MCF‐7 including some of which may explain the agonistic and antagonistic roles of the drug. Conclusions: The results indicate possible protective role of Tam against cardiovascular diseases as well as its involvement in G‐protein coupled receptors pathways that enhance breast tissue proliferation.
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- Extent
-
Online-Ressource
- Language
-
Englisch
- Bibliographic citation
-
Moonlighting Proteins and Cardiopathy in the Spatial Response of MCF‐7 Breast Cancer Cells to Tamoxifen ; volume:13 ; number:5 ; year:2019 ; extent:14
Proteomics / Clinical applications. Clinical applications ; 13, Heft 5 (2019) (gesamt 14)
- Creator
-
Alkhanjaf, Abdulrab Ahmed M.
Raggiaschi, Roberto
Crawford, Mark
Pinto, Gabriella
Godovac‐Zimmermann, Jasminka
- DOI
-
10.1002/prca.201900029
- URN
-
urn:nbn:de:101:1-2022080906220051784011
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:32 AM CEST
Data provider
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Alkhanjaf, Abdulrab Ahmed M.
- Raggiaschi, Roberto
- Crawford, Mark
- Pinto, Gabriella
- Godovac‐Zimmermann, Jasminka
Other Objects (12)
2-methoxyestradiol sensitizes tamoxifen-resistant MCF-7 breast cancer cells via downregulating HIF-1α
Anti-apoptotic effect of claudin-1 in tamoxifen-treated human breast cancer MCF-7 cells
Coffee decoction enhances tamoxifen proapoptotic activity on MCF-7 cells
Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Icariin induces apoptosis by suppressing autophagy in tamoxifen-resistant breast cancer cell line MCF-7/TAM
Correction to: Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Equol enhances tamoxifen’s anti-tumor activity by induction of caspase-mediated apoptosis in MCF-7 breast cancer cells
Metabolic response to XD14 treatment in human breast cancer cell line MCF-7
Inhibition of STAT3 enhances sensitivity to tamoxifen in tamoxifen-resistant breast cancer cells
Raptor localization predicts prognosis and tamoxifen response in estrogen receptor-positive breast cancer
Langzeitinkubation der Mammakarzinomzellinie MCF-7 M1 mit steigenden Konzentrationen von Tamoxifen und 3-OH-Tamoxifen (Droloxifen) : Resistenzentwicklung, Östrogen- und Progesteronrezeptorstatus, sowie ER-D5-Nachweis
Cytotoxic and chemomodulatory effects of Phyllanthus niruri in MCF-7 and MCF-7ADR breast cancer cells
2-methoxyestradiol sensitizes tamoxifen-resistant MCF-7 breast cancer cells via downregulating HIF-1α
Anti-apoptotic effect of claudin-1 in tamoxifen-treated human breast cancer MCF-7 cells
Coffee decoction enhances tamoxifen proapoptotic activity on MCF-7 cells
Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Icariin induces apoptosis by suppressing autophagy in tamoxifen-resistant breast cancer cell line MCF-7/TAM
Correction to: Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Equol enhances tamoxifen’s anti-tumor activity by induction of caspase-mediated apoptosis in MCF-7 breast cancer cells
Metabolic response to XD14 treatment in human breast cancer cell line MCF-7
Inhibition of STAT3 enhances sensitivity to tamoxifen in tamoxifen-resistant breast cancer cells
Raptor localization predicts prognosis and tamoxifen response in estrogen receptor-positive breast cancer
Langzeitinkubation der Mammakarzinomzellinie MCF-7 M1 mit steigenden Konzentrationen von Tamoxifen und 3-OH-Tamoxifen (Droloxifen) : Resistenzentwicklung, Östrogen- und Progesteronrezeptorstatus, sowie ER-D5-Nachweis
Cytotoxic and chemomodulatory effects of Phyllanthus niruri in MCF-7 and MCF-7ADR breast cancer cells
2-methoxyestradiol sensitizes tamoxifen-resistant MCF-7 breast cancer cells via downregulating HIF-1α
Anti-apoptotic effect of claudin-1 in tamoxifen-treated human breast cancer MCF-7 cells
Coffee decoction enhances tamoxifen proapoptotic activity on MCF-7 cells
Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Icariin induces apoptosis by suppressing autophagy in tamoxifen-resistant breast cancer cell line MCF-7/TAM
Correction to: Heregulin β1 drives gefitinib-resistant growth and invasion in tamoxifen-resistant MCF-7 breast cancer cells
Equol enhances tamoxifen’s anti-tumor activity by induction of caspase-mediated apoptosis in MCF-7 breast cancer cells
Metabolic response to XD14 treatment in human breast cancer cell line MCF-7
Inhibition of STAT3 enhances sensitivity to tamoxifen in tamoxifen-resistant breast cancer cells
Raptor localization predicts prognosis and tamoxifen response in estrogen receptor-positive breast cancer
Langzeitinkubation der Mammakarzinomzellinie MCF-7 M1 mit steigenden Konzentrationen von Tamoxifen und 3-OH-Tamoxifen (Droloxifen) : Resistenzentwicklung, Östrogen- und Progesteronrezeptorstatus, sowie ER-D5-Nachweis