ArticleOncogene2005
ERK1/2 inhibition increases antiestrogen treatment efficacy by interfering with hypoxia-induced downregulation of ERalpha: a combination therapy potentially targeting hypoxic and dormant tumor cells.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer.Future oncology (London, England) · 2014Trial
- Outlook and opportunities for engineered environments of breast cancer dormancy.Science advances · 2024Review
- The role of mitochondrial/metabolic axis in development of tamoxifen resistance in breast cancer.Human cell · 2023Review
- ERK MAP Kinase Signaling Regulates RAR Signaling to Confer Retinoid Resistance on Breast Cancer Cells.Cancers · 2022Article
- Article
- Review
- Metabolic/hypoxial axis predicts tamoxifen resistance in breast cancer.Scientific reports · 2022Article
- Conducive target range of breast cancer: Hypoxic tumor microenvironment.Frontiers in oncology · 2022Review
- Oxygen and metabolic reprogramming in the tumor microenvironment influences metastasis homing.Cancer biology & therapy · 2021Review
- Identification of key genes involved in tamoxifen-resistant breast cancer using bioinformatics analysis.Translational cancer research · 2021Article
- Hypoxia in Breast Cancer-Scientific Translation to Therapeutic and Diagnostic Clinical Applications.Frontiers in oncology · 2021Review
- Comparison of protein expression between formalin-fixed core-cut biopsies and surgical excision specimens using a novel multiplex approach.Breast cancer research and treatment · 2019Article
- Integrated molecular analysis of Tamoxifen-resistant invasive lobular breast cancer cells identifies MAPK and GRM/mGluR signaling as therapeutic vulnerabilities.Molecular and cellular endocrinology · 2018Article
- Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT.International journal of molecular sciences · 2018Review
- Activating HER3 mutations in breast cancer.Oncotarget · 2018Article
- Genome-independent hypoxic repression of estrogen receptor alpha in breast cancer cells.BMC cancer · 2017Article
- Associations of proteins relevant to MAPK signaling pathway (p38MAPK-1,HIF-1 and HO-1) with coronary lesion characteristics and prognosis of peri-menopausal women.Lipids in health and disease · 2016Article
- Mitochondria-Translocated PGK1 Functions as a Protein Kinase to Coordinate Glycolysis and the TCA Cycle in Tumorigenesis.Molecular cell · 2016Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor hypoxia is associated with cancer invasiveness, metastasis and treatment failure. Recent data suggest that the major target for endocrine treatment in breast cancer, ERalpha, is downregulated during hypoxia, but the mechanism behind this remains unknown. MAPK signaling as well as ERalpha regulation has earlier been independently linked to hypoxia and we now demonstrate HIF-1alpha and ERK1/2-activation in vivo towards the necrotic zone in DCIS of the breast, parallel with ERalpha downregulation. Hypoxia further caused transcriptional downregulation of ERalpha via activation of ERK1/2 in cell lines and, importantly, MEK1/2 inhibitors (U0126 or PD184352) or ERK1/2 suppression by siRNA partially restored the ERalpha expression. U0126 combined with tamoxifen accordingly produced an increased efficacy of the anti-estrogens during hypoxia. Based on these findings, we suggest a promising novel therapy for ERalpha-positive breast cancer where a combination of endocrine treatment and ERK1/2 inhibitors may increase treatment response by improved targeting of dormant hypoxic tumor cells.
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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.