ArticleInternational journal of molecular sciences2019
Oestrogen Non-Genomic Signalling is Activated in Tamoxifen-Resistant Breast Cancer.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Role of PRMT1 and PRMT5 in Breast Cancer.International journal of molecular sciences · 2024Review
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- Regulation of Bcl-2 Family Proteins in Estrogen Receptor-Positive Breast Cancer and Their Implications in Endocrine Therapy.Cancers · 2022Review
- Identification of potential target genes of honokiol in overcoming breast cancer resistance to tamoxifen.Frontiers in oncology · 2022Article
- Decoding the Therapeutic Implications of the ERα Stability and Subcellular Distribution in Breast Cancer.Frontiers in endocrinology · 2022Review
- Towards Unravelling the Role of ERα-Targeting miRNAs in the Exosome-Mediated Transferring of the Hormone Resistance.Molecules (Basel, Switzerland) · 2021Article
- Structure, Activity, and Function of PRMT1.Life (Basel, Switzerland) · 2021Review
- Analysis of genomic and non-genomic signaling of estrogen receptor in PDX models of breast cancer treated with a combination of the PI3K inhibitor alpelisib (BYL719) and fulvestrant.Breast cancer research : BCR · 2021Article
- Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer.Breast cancer research : BCR · 2020Article
- The Role of ERα36 in Development and Tumor Malignancy.International journal of molecular sciences · 2020Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Endocrine therapies targeting oestrogen signalling have significantly improved breast cancer management. However, their efficacy is limited by intrinsic and acquired resistance to treatment, which remains a major challenge for oestrogen receptor α (ERα)-positive tumours. Though many studies using in vitro models of endocrine resistance have identified putative actors of resistance, no consensus has been reached. We demonstrated previously that oestrogen non-genomic signalling, characterized by the formation of the ERα/Src/PI3K complex, is activated in aggressive breast cancers (BC). We wondered herein whether the activation of this pathway is also involved in resistance to endocrine therapies. We studied the interactions between ERα and Src or PI3K by proximity ligation assay (PLA) in in-vitro and in-vivo endocrine therapy-resistant breast cancer models. We reveal an increase in ERα/Src and ERα/PI3K interactions in patient-derived xenografts (PDXs) with acquired resistance to tamoxifen, as well as in tamoxifen-resistant MCF-7 cells compared to parental counterparts. Moreover, no interactions were observed in breast cancer cells resistant to other endocrine therapies. Finally, the use of a peptide inhibiting the ERα-Src interaction partially restored tamoxifen sensitivity in resistant cells, suggesting that such components could constitute promising targets to circumvent resistance to tamoxifen in BC.
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