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Involvement of multiple cellular pathways in regulating resistance to tamoxifen in BIK-suppressed MCF-7 cells

Majority of women with estrogen receptor (ER)-positive breast cancers initially respond to hormone therapies such as tamoxifen (TAM; antagonist of estrogen). However, many tumors eventually become resistant to TAM. Therefore, understanding the various cellular components involved in causing resistan... Full description

Journal Title: Tumor biology 2015-04-11, Vol.36 (9), p.6991-7005
Main Author: Viedma-Rodríguez, Rubí
Other Authors: Ruiz Esparza-Garrido, Ruth , Baiza-Gutman, Luis Arturo , Velázquez-Flores, Miguel Ángel , García-Carrancá, Alejandro , Salamanca-Gómez, Fabio , Arenas-Aranda, Diego
Format: Electronic Article Electronic Article
Language: English
Subjects:
RNA
Quelle: Alma/SFX Local Collection
Publisher: Dordrecht: Springer Netherlands
ID: ISSN: 1010-4283
Link: https://www.ncbi.nlm.nih.gov/pubmed/25861752
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title: Involvement of multiple cellular pathways in regulating resistance to tamoxifen in BIK-suppressed MCF-7 cells
format: Article
creator:
  • Viedma-Rodríguez, Rubí
  • Ruiz Esparza-Garrido, Ruth
  • Baiza-Gutman, Luis Arturo
  • Velázquez-Flores, Miguel Ángel
  • García-Carrancá, Alejandro
  • Salamanca-Gómez, Fabio
  • Arenas-Aranda, Diego
subjects:
  • 14-3-3 Proteins - genetics
  • Analysis
  • Apoptosis - drug effects
  • Apoptosis Regulatory Proteins - biosynthesis
  • Apoptosis Regulatory Proteins - genetics
  • Biomedical and Life Sciences
  • Biomedicine
  • Breast cancer
  • Breast Neoplasms - drug therapy
  • Breast Neoplasms - genetics
  • Breast Neoplasms - pathology
  • Cancer Research
  • Cell Cycle - drug effects
  • Cell Proliferation - drug effects
  • Cellular biology
  • DNA microarrays
  • Drug resistance
  • Drug Resistance, Neoplasm - genetics
  • Endocrine therapy
  • Estrogen
  • Estrogens
  • Estrogens - genetics
  • Female
  • Gene expression
  • Gene Expression Regulation, Neoplastic - drug effects
  • Genetic research
  • Humans
  • MCF-7 Cells
  • Membrane Proteins - biosynthesis
  • Membrane Proteins - genetics
  • Metabolic Networks and Pathways - drug effects
  • Neoplasm Proteins - biosynthesis
  • Research Article
  • RNA
  • Tamoxifen
  • Tamoxifen - administration & dosage
ispartof: Tumor biology, 2015-04-11, Vol.36 (9), p.6991-7005
description: Majority of women with estrogen receptor (ER)-positive breast cancers initially respond to hormone therapies such as tamoxifen (TAM; antagonist of estrogen). However, many tumors eventually become resistant to TAM. Therefore, understanding the various cellular components involved in causing resistance to TAM is of paramount importance in designing novel entities for efficacious hormone therapy. Previously, we found that suppression of BIK gene expression induced TAM resistance in MCF-7 breast cancer cells. In order to understand the response of these cells to TAM and its association with resistance, a microarray analysis of gene expression was performed in the BIK-suppressed MCF-7 cells and compared it to the TAM-only-treated cells (controls). Several genes participating in various cellular pathways were identified. Molecules identified in the drug resistance pathway were 14-3-3z or YWHAZ, WEE1, PRKACA, NADK, and HSP90AA 1. Further, genes involved in cell cycle control, apoptosis, and cell proliferation were also found differentially expressed in these cells. Transcriptional and translational analysis of key molecules such as STAT2, AKT 3, and 14-3-3z revealed similar changes at the messenger RNA (mRNA) as well as at the protein level. Importantly, there was no cytotoxic effect of TAM on BIK-suppressed MCF-7 cells. Further, these cells were not arrested at the G0-G1 phase of the cell cycle although 30 % of BIK-suppressed cells were arrested at the G2 phase of the cycle on TAM treatment. Furthermore, we found a relevant interaction between 14-3-3z and WEE1, suggesting that the cytotoxic effect of TAM was prevented in BIK-suppressed cells because this interaction leads to transitory arrest in the G2 phase leading to the repair of damaged DNA and allowing the cells to proliferate.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 1010-4283
fulltext: fulltext
issn:
  • 1010-4283
  • 1423-0380
url: Link


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titleInvolvement of multiple cellular pathways in regulating resistance to tamoxifen in BIK-suppressed MCF-7 cells
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creatorViedma-Rodríguez, Rubí ; Ruiz Esparza-Garrido, Ruth ; Baiza-Gutman, Luis Arturo ; Velázquez-Flores, Miguel Ángel ; García-Carrancá, Alejandro ; Salamanca-Gómez, Fabio ; Arenas-Aranda, Diego
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descriptionMajority of women with estrogen receptor (ER)-positive breast cancers initially respond to hormone therapies such as tamoxifen (TAM; antagonist of estrogen). However, many tumors eventually become resistant to TAM. Therefore, understanding the various cellular components involved in causing resistance to TAM is of paramount importance in designing novel entities for efficacious hormone therapy. Previously, we found that suppression of BIK gene expression induced TAM resistance in MCF-7 breast cancer cells. In order to understand the response of these cells to TAM and its association with resistance, a microarray analysis of gene expression was performed in the BIK-suppressed MCF-7 cells and compared it to the TAM-only-treated cells (controls). Several genes participating in various cellular pathways were identified. Molecules identified in the drug resistance pathway were 14-3-3z or YWHAZ, WEE1, PRKACA, NADK, and HSP90AA 1. Further, genes involved in cell cycle control, apoptosis, and cell proliferation were also found differentially expressed in these cells. Transcriptional and translational analysis of key molecules such as STAT2, AKT 3, and 14-3-3z revealed similar changes at the messenger RNA (mRNA) as well as at the protein level. Importantly, there was no cytotoxic effect of TAM on BIK-suppressed MCF-7 cells. Further, these cells were not arrested at the G0-G1 phase of the cell cycle although 30 % of BIK-suppressed cells were arrested at the G2 phase of the cycle on TAM treatment. Furthermore, we found a relevant interaction between 14-3-3z and WEE1, suggesting that the cytotoxic effect of TAM was prevented in BIK-suppressed cells because this interaction leads to transitory arrest in the G2 phase leading to the repair of damaged DNA and allowing the cells to proliferate.
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subject14-3-3 Proteins - genetics ; Analysis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - biosynthesis ; Apoptosis Regulatory Proteins - genetics ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cancer Research ; Cell Cycle - drug effects ; Cell Proliferation - drug effects ; Cellular biology ; DNA microarrays ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Endocrine therapy ; Estrogen ; Estrogens ; Estrogens - genetics ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic research ; Humans ; MCF-7 Cells ; Membrane Proteins - biosynthesis ; Membrane Proteins - genetics ; Metabolic Networks and Pathways - drug effects ; Neoplasm Proteins - biosynthesis ; Research Article ; RNA ; Tamoxifen ; Tamoxifen - administration & dosage
ispartofTumor biology, 2015-04-11, Vol.36 (9), p.6991-7005
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5Salamanca-Gómez, Fabio
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descriptionMajority of women with estrogen receptor (ER)-positive breast cancers initially respond to hormone therapies such as tamoxifen (TAM; antagonist of estrogen). However, many tumors eventually become resistant to TAM. Therefore, understanding the various cellular components involved in causing resistance to TAM is of paramount importance in designing novel entities for efficacious hormone therapy. Previously, we found that suppression of BIK gene expression induced TAM resistance in MCF-7 breast cancer cells. In order to understand the response of these cells to TAM and its association with resistance, a microarray analysis of gene expression was performed in the BIK-suppressed MCF-7 cells and compared it to the TAM-only-treated cells (controls). Several genes participating in various cellular pathways were identified. Molecules identified in the drug resistance pathway were 14-3-3z or YWHAZ, WEE1, PRKACA, NADK, and HSP90AA 1. Further, genes involved in cell cycle control, apoptosis, and cell proliferation were also found differentially expressed in these cells. Transcriptional and translational analysis of key molecules such as STAT2, AKT 3, and 14-3-3z revealed similar changes at the messenger RNA (mRNA) as well as at the protein level. Importantly, there was no cytotoxic effect of TAM on BIK-suppressed MCF-7 cells. Further, these cells were not arrested at the G0-G1 phase of the cell cycle although 30 % of BIK-suppressed cells were arrested at the G2 phase of the cycle on TAM treatment. Furthermore, we found a relevant interaction between 14-3-3z and WEE1, suggesting that the cytotoxic effect of TAM was prevented in BIK-suppressed cells because this interaction leads to transitory arrest in the G2 phase leading to the repair of damaged DNA and allowing the cells to proliferate.
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014-3-3 Proteins - genetics
1Analysis
2Apoptosis - drug effects
3Apoptosis Regulatory Proteins - biosynthesis
4Apoptosis Regulatory Proteins - genetics
5Biomedical and Life Sciences
6Biomedicine
7Breast cancer
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11Cancer Research
12Cell Cycle - drug effects
13Cell Proliferation - drug effects
14Cellular biology
15DNA microarrays
16Drug resistance
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18Endocrine therapy
19Estrogen
20Estrogens
21Estrogens - genetics
22Female
23Gene expression
24Gene Expression Regulation, Neoplastic - drug effects
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27MCF-7 Cells
28Membrane Proteins - biosynthesis
29Membrane Proteins - genetics
30Metabolic Networks and Pathways - drug effects
31Neoplasm Proteins - biosynthesis
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35Tamoxifen - administration & dosage
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1Ruiz Esparza-Garrido, Ruth
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5Salamanca-Gómez, Fabio
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atitleInvolvement of multiple cellular pathways in regulating resistance to tamoxifen in BIK-suppressed MCF-7 cells
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date2015-04-11
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abstractMajority of women with estrogen receptor (ER)-positive breast cancers initially respond to hormone therapies such as tamoxifen (TAM; antagonist of estrogen). However, many tumors eventually become resistant to TAM. Therefore, understanding the various cellular components involved in causing resistance to TAM is of paramount importance in designing novel entities for efficacious hormone therapy. Previously, we found that suppression of BIK gene expression induced TAM resistance in MCF-7 breast cancer cells. In order to understand the response of these cells to TAM and its association with resistance, a microarray analysis of gene expression was performed in the BIK-suppressed MCF-7 cells and compared it to the TAM-only-treated cells (controls). Several genes participating in various cellular pathways were identified. Molecules identified in the drug resistance pathway were 14-3-3z or YWHAZ, WEE1, PRKACA, NADK, and HSP90AA 1. Further, genes involved in cell cycle control, apoptosis, and cell proliferation were also found differentially expressed in these cells. Transcriptional and translational analysis of key molecules such as STAT2, AKT 3, and 14-3-3z revealed similar changes at the messenger RNA (mRNA) as well as at the protein level. Importantly, there was no cytotoxic effect of TAM on BIK-suppressed MCF-7 cells. Further, these cells were not arrested at the G0-G1 phase of the cell cycle although 30 % of BIK-suppressed cells were arrested at the G2 phase of the cycle on TAM treatment. Furthermore, we found a relevant interaction between 14-3-3z and WEE1, suggesting that the cytotoxic effect of TAM was prevented in BIK-suppressed cells because this interaction leads to transitory arrest in the G2 phase leading to the repair of damaged DNA and allowing the cells to proliferate.
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