Evidence map›Paper›PMID 41151866›Full record

ArticleCancer genomics & proteomics

BMP1 Appears to be Involved in GPER1-mediated Progression and Tamoxifen Resistance of Luminal A Breast Cancer Cells.

Katharina Wert, Johanna Jentsch, Julia Gallwas, Carsten Gründker

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Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Katharina Wert *Department of Gynecology and Obstetrics, University Medical Center Göttingen, Göttingen, Germany.
Johanna Jentsch *Department of Gynecology and Obstetrics, University Medical Center Göttingen, Göttingen, Germany.
Julia GallwasDepartment of Gynecology and Obstetrics, University Medical Center Göttingen, Göttingen, Germany.
Carsten GründkerDepartment of Gynecology and Obstetrics, University Medical Center Göttingen, Göttingen, Germany grundker@med.uni-goettingen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimBone morphogenetic protein 1 (BMP1) plays a role in the activation of both transforming growth factor-β (TGFβ) and BMP signaling pathways. We investigated whether BMP1 is involved in G-protein coupled estrogen receptor 1 (GPER1)-regulated progression of luminal A-type breast cancer cells. MATERIALS AND

methodsPublicly available transcriptomic data from MCF7 breast cancer cells treated with the selective GPER1 agonist G1 were analyzed and the results, in particular the altered BMP1 expression, were validated by qPCR. Signs of epithelial-mesenchymal transition (EMT) were visualized by immune cytology. Invasion was quantified by modified Boyden chamber assay. Tamoxifen-resistant sublines of the MCF7 and T47D cell lines were established.

resultsActivation of GPER1 by the agonist G1 increased the expression of BMP1 in MCF7 and T47D luminal A breast cancer cells. In addition, EMT and invasion was enhanced after GPER1 activation. This effect could be prevented in part by the BMP1 inhibitor UK383367. Tamoxifen-resistant MCF7-TR and T47D-TR cells exhibited higher BMP1 expression, signs of EMT and enhanced invasiveness compared to their tamoxifen-sensitive wild type. Blocking GPER1 in MCF7-TR and T47D-TR cells using the antagonist G36 led to reduction in BMP1 expression, a slight decrease in EMT, reduced cell invasion, and increased sensitivity to tamoxifen.

conclusionBMP1 appears to be involved in GPER1-mediated progression of luminal A breast cancer cells. In addition, BMP1 may play a role in tamoxifen-resistance.

Indexed as

Bone Morphogenetic Protein 1Breast NeoplasmsDrug Resistance, NeoplasmReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenAntineoplastic Agents, HormonalCell Line, TumorDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsAntineoplastic Agents, HormonalBone Morphogenetic Protein 1GPER1 protein, humanReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenBMP1Bone morphogenetic protein 1GPER1G-protein coupled estrogen receptor 1luminal A breast cancertamoxifen-resistance

Identifiers

PMID41151866
PMCPMC12577600

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.