RETRACTED: Predictive and prognostic value of ER-α36 expression in breast cancer patients treated with chemotherapy

Yu, Lanfang; Wei, Ke; Wang, Yanli; Ding, Wei; Wang, Bo; Huang, Sufang; Chen, Jing; Wang, Xiaoting; Wang, Zhaoyi; Shen, Peng

doi:10.1016/j.steroids.2014.03.003

Cited by 8 publications

(4 citation statements)

References 30 publications

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“…5). Regarding ER expression, the results of endocrine therapies demonstrated that tumor overexpressing ERa36 has been proven to slow the progression with chemotherapy, and ERa36 negative tumors that received neoadjuvant chemotherapy have better prognosis [150]. For example, tamoxifen therapy has limited efficacy in women who are positive for ERa36 [151], even in ERa negative BC patients, suggesting that tamoxifen is unable to prevent the non-genomic signaling pathway induced by the ERa36 [111].…”

Section: Specific Role Of Steroid Receptors In Bcmentioning

confidence: 99%

The role of sex hormones and steroid receptors on female reproductive cancers

et al. 2017

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Sex steroids have been widely described to be associated with a number of human diseases, including hormone-dependent tumors. Several studies have been concerned about the factors regulating the availability of sex steroids and its importance in the pathophysiological aspects of the reproductive cancers in women. In premenopausal women, large fluctuations in the concentration of circulating estradiol (E2) and progesterone (P4) orchestrate many events across the menstrual cycle. After menopause, the levels of circulating E2 and P4 decline but remain at high concentration in the peripheral tissues. Notably, there is a strong relationship between circulating sex hormones and female reproductive cancers (e.g. ovarian, breast, and endometrial cancers). These hormones activate a number of specific signaling pathways after binding either to estrogen receptors (ERs), especially ERα, ERα36, and ERβ or progesterone receptors (PRs). Importantly, the course of the disease will depend on particular transactivation pathway. Identifying ER- or PR-positive tumors will benefit patients in terms of proper endocrine therapy. Based on hormonal responsiveness, effective prevention methods for ovarian, breast, and endometrial cancers represent a special opportunity for women at risk of malignancies. Hormone replacement therapy (HRT) might significantly increase the risk of these cancer types, and endocrine treatments targeting ER signaling may be helpful against E2-dependent tumors. This review will present the role of sex steroids and their receptors associated with the risk of developing female reproductive cancers, with emphasis on E2 levels in pre and postmenopausal women. In addition, new therapeutic strategies for improving the survival rate outcomes in women will be addressed.

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Section: Specific Role Of Steroid Receptors In Bcmentioning

confidence: 99%

The role of sex hormones and steroid receptors on female reproductive cancers

et al. 2017

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“…Recently, Yu et al, (2014) reported that breast cancer patients with tumors highly expressing ER-36 less benefited from neoadjuvant chemotherapy and have worse prognosis, It was suggested that ER-36 may be used as a predictive biomarker for the efficacy of neoadjuvant chemotherapy, and the negative expression of ER-36 may be a favorable factor of prognosis in breast cancer patients treated with neoadjuvant chemotherapy.…”

Section: Er-36 In Er-negative Breast Cancer and Chemotherapy Resistancementioning

confidence: 99%

Estrogen receptor alpha-36 (ER-α36): A new player in human breast cancer

Wang

Yin

2015

Molecular and Cellular Endocrinology

138

124

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Prevailing wisdom is that estrogen receptor (ER)-α mediated genomic estrogen signaling is responsible for estrogen-stimulated cell proliferation and development of ER-positive breast cancer. However, accumulating evidence indicates that another estrogen signaling pathway, non-genomic or rapid estrogen signaling, also plays an important role in mitogenic estrogen signaling. Previously, our laboratory cloned a 36 kDa variant of ER-α, ER-α36, and found that ER-α36 is mainly expressed in the cytoplasm and at the plasma membrane. ER-α36 mediates rapid estrogen signaling and inhibits genomic estrogen signaling. In this review, we review and update the biological function of ER-α36 in ER-positive and -negative breast cancer, breast cancer stem/progenitor cells and tamoxifen resistance, potential interaction and cross-talk of ER-α36 with other ERs and growth factor receptors, and intracellular pathways of ER-α36-mediated rapid estrogen signaling. The potential function and underlying mechanism of ER-α in development of ER-positive breast cancer will also be discussed.

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“…ER-α36 is crucial in the carcinogenesis and aggressiveness of breast cancer; in addition, it explains why antiestrogen therapy loses efficacy in ER-positive breast cancer patients 20–22. These achievements imply that ER-α36 is a promising biomarker for diagnosis, prognosis, and treatment of various diseases, especially breast cancer 23–25. What’s more, it provides a novel pharmaceutical approach to individualized treatment of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

ER-α36: a novel biomarker and potential therapeutic target in breast cancer

Su¹,

Xu²,

Li³

et al. 2014

OTT

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Estrogen receptor-alpha36 (ER-α36) is a 36-kDa variant of estrogen receptor-alpha (ER-α) firstly identified and cloned by Wang et al in 2005. It lacks both transactivation domains (activation function 1 and activation function 2) and has different biological characteristics compared to traditional ER-α (ER-α66). ER-α36 primarily locates on plasma membrane and cytoplasm and functions as a mediator in the rapid membrane-initiated non-genomic signaling pathway. Additionally, it inhibits the traditional genomic signaling pathway mediated by ER-α66 in a dominant-negative pattern. Accumulating evidence has demonstrated that ER-α36 regulates the physiological function of various tissues. Thus, dysregulation of ER-α36 is closely associated with plenty of diseases including cancers. ER-α36 is recognized as a molecular abnormality which solidly correlates to carcinogenesis, aggressiveness, and therapeutic response of breast cancer. Additionally, special attention has been paid to the role of ER-α36 in endocrine therapy resistance. Therefore, ER-α36 provides a novel biomarker of great value for diagnosis, prognosis, and treatment of breast cancer. It may also be a potential therapeutic target for breast cancer patients, especially for those who are resistant to endocrine therapy. In this review, we will overview and update the biological characteristics, underlying mechanism, and function of ER-α36, focusing on its biological function in breast cancer and endocrine therapy resistance. We will evaluate its application value in clinical practice.

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RETRACTED: Predictive and prognostic value of ER-α36 expression in breast cancer patients treated with chemotherapy

Cited by 8 publications

References 30 publications

The role of sex hormones and steroid receptors on female reproductive cancers

The role of sex hormones and steroid receptors on female reproductive cancers

Estrogen receptor alpha-36 (ER-α36): A new player in human breast cancer

ER-α36: a novel biomarker and potential therapeutic target in breast cancer

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RETRACTED: Predictive and prognostic value of ER-α36 expression in breast cancer patients treated with chemotherapy

Cited by 8 publications

References 30 publications

The role of sex hormones and steroid receptors on female reproductive cancers

The role of sex hormones and steroid receptors on female reproductive cancers

Estrogen receptor alpha-36 (ER-α36): A new player in human breast cancer

ER-&alpha;36: a novel biomarker and potential therapeutic target in breast cancer

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ER-α36: a novel biomarker and potential therapeutic target in breast cancer