ArticleOncotarget2015
DMXL2 drives epithelial to mesenchymal transition in hormonal therapy resistant breast cancer through Notch hyper-activation.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
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- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- Genetic polymorphisms as predictors of the response of hepatocellular carcinoma patients to doxorubicin chemotherapy: a genome-wide association study.Frontiers in pharmacology · 2025Article
- Cytokeratin expression in breast cancer: from mechanisms, progression, diagnosis, and prognosis to therapeutic implications.Molecular & cellular oncology · 2025Review
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- Short- and long-term effects of radiation exposure at low dose and low dose rate in normal human VH10 fibroblasts.Frontiers in public health · 2023Article
- Genomic profiling identifies distinct genetic subtypes in extra-nodal natural killer/T-cell lymphoma.Leukemia · 2022Article
- A Joint Model of Random Forest and Artificial Neural Network for the Diagnosis of Endometriosis.Frontiers in genetics · 2022Article
- Study of Single Nucleotide Polymorphisms Associated with Breast Cancer Patients among Arab Ancestries.International journal of breast cancer · 2022Article
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- Tumor-Associated Macrophages: Critical Players in Drug Resistance of Breast Cancer.Frontiers in immunology · 2021Review
- RAVE and Rabconnectin-3 Complexes as Signal Dependent Regulators of Organelle Acidification.Frontiers in cell and developmental biology · 2021Review
- Spatial regulation and generation of diversity in signaling pathways.Journal of biosciences · 2021Review
- Nuclear Mechanisms Involved in Endocrine Resistance.Frontiers in oncology · 2021Review
- Overcoming Endocrine Resistance in Breast Cancer.Cancer cell · 2020Review
- Notch Signaling Pathway and Endocrine Resistance in Breast Cancer.Frontiers in pharmacology · 2020Review
- SREBP1 drives Keratin-80-dependent cytoskeletal changes and invasive behavior in endocrine-resistant ERα breast cancer.Nature communications · 2019Article
- Dual role of DMXL2 in olfactory information transmission and the first wave of spermatogenesis.PLoS genetics · 2019Article
- Monoamine oxidase-A activity is required for clonal tumorsphere formation by human breast tumor cells.Cellular & molecular biology letters · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The acquisition of endocrine therapy resistance in estrogen receptor α (ERα) breast cancer patients represents a major clinical problem. Notch signalling has been extensively linked to breast cancer especially in patients who fail to respond to endocrine therapy. Following activation, Notch intracellular domain is released and enters the nucleus where activates transcription of target genes. The numerous steps that cascade after activation of the receptor complicate using Notch as biomarker. Hence, this warrants the development of reliable indicators of Notch activity. DMXL2 is a novel regulator of Notch signalling not yet investigated in breast cancer. Here, we demonstrate that DMXL2 is overexpressed in a subset of endocrine therapy resistant breast cancer cell lines where it promotes epithelial to mesenchymal transition through hyper-activation of Notch signalling via V-ATPase dependent acidification. Following DMXL2 depletion or treatment with Bafilomycin A1, both EMT targets and Notch signalling pathway significantly decrease. We show for the first time that DMXL2 protein levels are significantly increased in ERα positive breast cancer patients that progress after endocrine therapy. Finally, we demonstrate that DMXL2 is a transmembrane protein with a potential extra-cellular domain. These findings identify DMXL2 as a novel, functional biomarker for ERα positive breast cancer.
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Registered trials
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.