Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma

Kuo Chiang Chen; Chih Ming Lin; Chi Jung Huang; Shao Kuan Chen; Sheng Tang Wu; Han-Sun Chiang; Wei Chi Ku

Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma

Kuo Chiang Chen, Chih Ming Lin, Chi Jung Huang, Shao Kuan Chen, Sheng Tang Wu, Han-Sun Chiang, Wei Chi Ku

Taipei Medical University Hospital

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

Abstract

Background: It has been proposed that 17-β- estradiol (E2) activates estrogen receptor and inhibits renal cell carcinoma (RCC) growth. In the present study we explored the role of E2 and ER in the regulation of RCC growth. Materials and Methods: The RCC cell line ACHN was treated by E2 combining with E2 antagonist Fulvestrant or ER knockdown, and cell growth was monitored. Quantitative phosphoproteomics was applied to study the E2 regulated non-genomic phosphorylation changes. Western blotting, immunofluorescence microscopy, and apoptosis assays were used for validation. Results: E2 induced ERdependent growth inhibition in RCC cell lines. Quantitative phosphoproteomics revealed that E2 induced both apoptosis and autophagy. Cellular apoptosis was confirmed by altered.

Original language	English
Pages (from-to)	219-230
Number of pages	12
Journal	Cancer Genomics and Proteomics
Volume	13
Issue number	3
Publication status	Published - May 1 2016

Keywords

17-β -estradiol
Apoptosis
Autophagy
Estrogen receptor
Quantitative phosphoproteomics
Renal cell carcinoma

ASJC Scopus subject areas

Genetics
Molecular Biology
Cancer Research
Biochemistry

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Cite this

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title = "Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma",

abstract = "Background: It has been proposed that 17-β- estradiol (E2) activates estrogen receptor and inhibits renal cell carcinoma (RCC) growth. In the present study we explored the role of E2 and ER in the regulation of RCC growth. Materials and Methods: The RCC cell line ACHN was treated by E2 combining with E2 antagonist Fulvestrant or ER knockdown, and cell growth was monitored. Quantitative phosphoproteomics was applied to study the E2 regulated non-genomic phosphorylation changes. Western blotting, immunofluorescence microscopy, and apoptosis assays were used for validation. Results: E2 induced ERdependent growth inhibition in RCC cell lines. Quantitative phosphoproteomics revealed that E2 induced both apoptosis and autophagy. Cellular apoptosis was confirmed by altered.",

keywords = "17-β -estradiol, Apoptosis, Autophagy, Estrogen receptor, Quantitative phosphoproteomics, Renal cell carcinoma",

author = "Chen, {Kuo Chiang} and Lin, {Chih Ming} and Huang, {Chi Jung} and Chen, {Shao Kuan} and Wu, {Sheng Tang} and Han-Sun Chiang and Ku, {Wei Chi}",

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TY - JOUR

T1 - Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma

AU - Chen, Kuo Chiang

AU - Lin, Chih Ming

AU - Huang, Chi Jung

AU - Chen, Shao Kuan

AU - Wu, Sheng Tang

AU - Chiang, Han-Sun

AU - Ku, Wei Chi

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Background: It has been proposed that 17-β- estradiol (E2) activates estrogen receptor and inhibits renal cell carcinoma (RCC) growth. In the present study we explored the role of E2 and ER in the regulation of RCC growth. Materials and Methods: The RCC cell line ACHN was treated by E2 combining with E2 antagonist Fulvestrant or ER knockdown, and cell growth was monitored. Quantitative phosphoproteomics was applied to study the E2 regulated non-genomic phosphorylation changes. Western blotting, immunofluorescence microscopy, and apoptosis assays were used for validation. Results: E2 induced ERdependent growth inhibition in RCC cell lines. Quantitative phosphoproteomics revealed that E2 induced both apoptosis and autophagy. Cellular apoptosis was confirmed by altered.

AB - Background: It has been proposed that 17-β- estradiol (E2) activates estrogen receptor and inhibits renal cell carcinoma (RCC) growth. In the present study we explored the role of E2 and ER in the regulation of RCC growth. Materials and Methods: The RCC cell line ACHN was treated by E2 combining with E2 antagonist Fulvestrant or ER knockdown, and cell growth was monitored. Quantitative phosphoproteomics was applied to study the E2 regulated non-genomic phosphorylation changes. Western blotting, immunofluorescence microscopy, and apoptosis assays were used for validation. Results: E2 induced ERdependent growth inhibition in RCC cell lines. Quantitative phosphoproteomics revealed that E2 induced both apoptosis and autophagy. Cellular apoptosis was confirmed by altered.

KW - 17-β -estradiol

KW - Apoptosis

KW - Autophagy

KW - Estrogen receptor

KW - Quantitative phosphoproteomics

KW - Renal cell carcinoma

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Dual roles of 17-β estradiol in estrogen receptor-dependent growth inhibition in renal cell carcinoma

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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