Estrogen-independent effects of ER-α36 in ER-negative breast cancer

Jing Zhang; Guangliang Li; Zhongqi Li; Xiongfei Yu; Yi Zheng; Ketao Jin; Haohao Wang; Yun Gong; Xiaoping Sun; Xiaodong Teng; Jiang Cao; Lisong Teng

doi:10.1016/j.steroids.2012.02.013

Estrogen-independent effects of ER-α36 in ER-negative breast cancer

Jing Zhang, Guangliang Li, Zhongqi Li, Xiongfei Yu, Yi Zheng, Ketao Jin, Haohao Wang, Yun Gong, Xiaoping Sun, Xiaodong Teng, Jiang Cao, Lisong Teng

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

37 Scopus citations

Abstract

Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.

Original language	English (US)
Pages (from-to)	666-673
Number of pages	8
Journal	Steroids
Volume	77
Issue number	6
DOIs	https://doi.org/10.1016/j.steroids.2012.02.013
State	Published - May 2012

Keywords

Breast cancer
Estrogen receptor-alpha 36
Metastasis
Paclitaxel

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Endocrinology
Pharmacology
Clinical Biochemistry
Organic Chemistry

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10.1016/j.steroids.2012.02.013

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title = "Estrogen-independent effects of ER-α36 in ER-negative breast cancer",

abstract = "Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.",

keywords = "Breast cancer, Estrogen receptor-alpha 36, Metastasis, Paclitaxel",

author = "Jing Zhang and Guangliang Li and Zhongqi Li and Xiongfei Yu and Yi Zheng and Ketao Jin and Haohao Wang and Yun Gong and Xiaoping Sun and Xiaodong Teng and Jiang Cao and Lisong Teng",

note = "Funding Information: This work was supported by the State Key Basic Research and Development Program of China (973 Program, Grant No. 2009CB521704 ), National High-tech Research & Development Program of China (863 Program, Grant No. 2006AA02A245 ), National Natural Science Foundation of China (Grant No. 81000894 ) and Zhejiang Provincial Science and Technology Project (Grant No. 2009C13021 ). ",

year = "2012",

month = may,

doi = "10.1016/j.steroids.2012.02.013",

language = "English (US)",

volume = "77",

pages = "666--673",

journal = "Steroids",

issn = "0039-128X",

publisher = "Elsevier Inc.",

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T1 - Estrogen-independent effects of ER-α36 in ER-negative breast cancer

AU - Zhang, Jing

AU - Li, Guangliang

AU - Li, Zhongqi

AU - Yu, Xiongfei

AU - Zheng, Yi

AU - Jin, Ketao

AU - Wang, Haohao

AU - Gong, Yun

AU - Sun, Xiaoping

AU - Teng, Xiaodong

AU - Cao, Jiang

AU - Teng, Lisong

N1 - Funding Information: This work was supported by the State Key Basic Research and Development Program of China (973 Program, Grant No. 2009CB521704 ), National High-tech Research & Development Program of China (863 Program, Grant No. 2006AA02A245 ), National Natural Science Foundation of China (Grant No. 81000894 ) and Zhejiang Provincial Science and Technology Project (Grant No. 2009C13021 ).

PY - 2012/5

Y1 - 2012/5

N2 - Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.

AB - Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.

KW - Breast cancer

KW - Estrogen receptor-alpha 36

KW - Metastasis

KW - Paclitaxel

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Estrogen-independent effects of ER-α36 in ER-negative breast cancer

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