ArticleOncotarget2017
Mitochondrial "power" drives tamoxifen resistance: NQO1 and GCLC are new therapeutic targets in breast cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
- NQO1 as a predictor of response to adjuvant GemCap treatment for pancreatic cancer.Journal of the National Cancer Institute · 2026Article
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Trophoblast cell response to periodontal pathogens unveils oxidative stress networks between periodontitis and pre-eclampsia: Mendelian randomization, transcriptomic analysis, and cellular experimental validation.European journal of medical research · 2025Article
- Patient-derived organotypic tissue cultures as a platform to evaluate metabolic reprogramming in breast cancer patients.The Journal of biological chemistry · 2025Article
- Patient-derived response estimates from zero-passage organoids of luminal breast cancer.Breast cancer research : BCR · 2024Article
- High mitochondrial DNA content is a key determinant of stemness, proliferation, cell migration, and cancer metastasis in vivo.Cell death & disease · 2024Article
- Inverse FASN and LDHA correlation drives metabolic resistance in breast cancer.Journal of translational medicine · 2024Article
- Patient-derived response estimates from zero-passage organoids of luminal breast cancer.bioRxiv : the preprint server for biology · 2024Article
- Article
- Role of monocarboxylate transporter I/lactate dehydrogenase B-mediated lactate recycling in tamoxifen-resistant breast cancer cells.Archives of pharmacal research · 2023Article
- The role of mitochondrial/metabolic axis in development of tamoxifen resistance in breast cancer.Human cell · 2023Review
- Identifying prognostic subgroups of luminal-A breast cancer using deep autoencoders and gene expressions.PLoS computational biology · 2023Article
- Computational drug repositioning for the identification of new agents to sensitize drug-resistant breast tumors across treatments and receptor subtypes.Frontiers in oncology · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Ferroptosis and Its Multifaceted Role in Cancer: Mechanisms and Therapeutic Approach.Antioxidants (Basel, Switzerland) · 2022Review
- Carnosic Acid Encapsulated in Albumin Nanoparticles Induces Apoptosis in Breast and Colorectal Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- Drug Metabolism for the Identification of Clinical Biomarkers in Breast Cancer.International journal of molecular sciences · 2022Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we identified two new molecular targets, which are functionally sufficient to metabolically confer the tamoxifen-resistance phenotype in human breast cancer cells. Briefly, ~20 proteins were first selected as potential candidates, based on unbiased proteomics analysis, using tamoxifen-resistant cell lines. Then, the cDNAs of the most promising candidates were systematically transduced into MCF-7 cells. Remarkably, NQO1 and GCLC were both functionally sufficient to autonomously confer a tamoxifen-resistant metabolic phenotype, characterized by i) increased mitochondrial biogenesis, ii) increased ATP production and iii) reduced glutathione levels. Thus, we speculate that pharmacological inhibition of NQO1 and GCLC may be new therapeutic strategies for overcoming tamoxifen-resistance in breast cancer patients. In direct support of this notion, we demonstrate that treatment with a known NQO1 inhibitor (dicoumarol) is indeed sufficient to revert the tamoxifen-resistance phenotype. As such, these findings could have important translational significance for the prevention of tumor recurrence in ER(+) breast cancers, which is due to an endocrine resistance phenotype. Importantly, we also show here that NQO1 has significant prognostic value as a biomarker for the prediction of tumor recurrence. More specifically, higher levels of NQO1 mRNA strongly predict patient relapse in high-risk ER(+) breast cancer patients receiving endocrine therapy (mostly tamoxifen; H.R. > 2.15; p = 0.007).
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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.