Tamoxifen and ERα36: Fertilizing the seeds of breast cancer metastasis

Burness, Monika L.; Wicha, Max S.

doi:10.1038/s41422-018-0028-4

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…This deleterious effect appears to be largely related to the agonistic/ inducing effects of tamoxifen on ERα36 which lead to the activation of various signaling pathways involved in metastatic properties [53]. Indeed, treating MDA-MB 436 breast cancer cells with tamoxifen leads to the detection of an ERα36 modified heavy form of into the nucleus, which is associated with the induction the mammary cancer stem cell marker ALDH1 [53,104]. However, the mechanism underlying this ERα36-dependent nuclear localization and transcriptional regulation remains to be determined.…”

Section: Future Prospectsmentioning

confidence: 99%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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Estrogen nuclear receptors, represented by the canonical forms ERα66 and ERβ1, are the main mediators of the estrogen-dependent pathophysiology in mammals. However, numerous isoforms have been identified, stimulating unconventional estrogen response pathways leading to complex cellular and tissue responses. The estrogen receptor variant, ERα36, was cloned in 2005 and is mainly described in the literature to be involved in the progression of mammary tumors and in the acquired resistance to anti-estrogen drugs, such as tamoxifen. In this review, we will first specify the place that ERα36 currently occupies within the diversity of nuclear and membrane estrogen receptors. We will then report recent data on the impact of ERα36 expression and/or activity in normal breast and testicular cells, but also in different types of tumors including mammary tumors, highlighting why ERα36 can now be considered as a marker of malignancy. Finally, we will explain how studying the regulation of ERα36 expression could provide new clues to counteract resistance to cancer treatments in hormone-sensitive tumors.

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Section: Future Prospectsmentioning

confidence: 99%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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“…2005, Wang and his colleagues identified a ERα66 variant named ERα36 [5], It is expressed in many breast cancer cells, especially highly expressed in TAM-resistant cell lines and triple-negative breast cancer [6]. Studies have shown that expression of ERα36 is related to the prognosis, metastasis and drug resistance of breast cancer [7,8]. It also stimulates the activation of PI3K/AKT and MAPK/ERK pathway [9].…”

Section: Introductionmentioning

confidence: 99%

Curcumol Inhibit Breast Cancer Growth Via NCL/ERα36 And PI3K/AKT Pathway

Wei

Wang

Dou

et al. 2021

Preprint

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Purpose: This study is to investigate the effect and mechanism of curcumol on ERα36 positive breast cancer cells, and the relationship between curcumol’s target protein nucleolin (NCL) and ERα36. Methods: The anti-tumor effect of curcumol were quantified via MTT assay, colony formation and cycle arrest respectively. The expression of ERα36, NCL and the proteins involved in PI3K/AKT signaling were evaluated by western blotting. The interaction between two proteins were detected using co-immunoprecipitation (Co-IP) and immunofluorescence assay. Mouse xenograft model was established to verify the role of ERα36 in breast cancer cells and curcumol’s effect on ERα36 positive cancer cells. Results: Curcumol inhibited the cell growth, caused cell cycle arrest, decreased cell cycle related-proteins and inactivated PI3K/AKT pathway in ERα36 positive breast cancer cells. There is a positive correlation between NCL and ERα36 in breast cancer cells. In addition, ERα36 bound to NCL, the two proteins were distributed in the nucleus, cytoplasm and on the plasma membrane, where their expression were obviously decreased by curcumol. Moreover, NCL silenced by NCL siRNA blocked the cell cycle progress and inhibited the activation of PI3K/AKT in MDA-MB-231 cells, while overexpressed ERα36 increased the expression of NCL, promoted cell cycle progress and enhanced the activity of PI3K/AKT in MCF-7 cells. NCL knockdown or ERα36 overexpressed all attenuated the effect of curcumol on breast cancer cells. Conclusion: Curcumol reduced the proliferation of breast cancer cells by targeting NCL/ERα36 and inactivated PI3K/AKT pathway.

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“…We can anticipate future studies comparing compliance, imaging, microbiome, and breast tissue biomarker change in individuals receiving low versus standard doses. Tamoxifen enhances NFkB and breast stem cell activity through a variety of molecular mechanisms which can result in tamoxifen resistance (14,15). Studies in which low-dose tamoxifen is paired with other well-tolerated agents targeting processes associated with endocrine therapy resistance should be expected.…”

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confidence: 99%

Tamoxifen: Will Less Equal More in Women with Precancerous Breast Disease?

Fabian

2021

Clinical Cancer Research

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Similar risk reduction but fewer side effects would predict more uptake and compliance with low (5 mg) versus full (20 mg) dose tamoxifen. Benefit with low dose is demonstrated for perimenopausal/postmenopausal women with intraepithelial neoplasia and high lesion Ki-67. Longer follow-up needed to determine benefit with low lesion Ki-67. See related article by DeCensi et al., p. 3576

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Tamoxifen and ERα36: Fertilizing the seeds of breast cancer metastasis

Cited by 4 publications

References 11 publications

The Role of ERα36 in Development and Tumor Malignancy

The Role of ERα36 in Development and Tumor Malignancy

Curcumol Inhibit Breast Cancer Growth Via NCL/ERα36 And PI3K/AKT Pathway

Tamoxifen: Will Less Equal More in Women with Precancerous Breast Disease?

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