ArticleBMC cancer2018
Association of tamoxifen resistance and lipid reprogramming in breast cancer.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 216 citations in OpenAlex.
- Molecular Mechanisms Underlying Recurrence in Triple-Positive Breast Cancer (ER+/PR+/HER2+) and Potential Repurposing of Multi-Target Inhibitors.International journal of molecular sciences · 2026Review
- Integrating multi-omics and clinical management in breast cancer: a comprehensive review.Discover oncology · 2026Review
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Declined RTN3 stabilizes DHCR7 to induce cholesterol-dependent tumor progression and MEK inhibitors insensitivity in thyroid cancer.Cell death & disease · 2026Article
- Targeting fatty acid metabolism for cancer therapy.Fundamental research · 2026Review
- Article
- The Impact of IGFBP6 Knockdown on Cholesterol Metabolism in Breast Cancer Cells.Current medicinal chemistry · 2026Article
- Lipid Metabolism and Breast Cancer Therapy: An Integrative Literature Review.Breast cancer (Dove Medical Press) · 2026Review
- Immune evasion driven by lipid metabolic reprogramming in endocrine-resistant HRFrontiers in immunology · 2026Review
- A lipid metabolism-related gene signature predicts prognosis after tamoxifen treatment in ER + breast cancer and reflects tumor microenvironment heterogeneity through single-cell analysis.BMC medical genomics · 2025Article
- ZMIZ1 lactylation induces tamoxifen resistance in breast cancer through increasing transcriptional activity of Nanog to impact cell stemness and cholesterol uptake.Cell biology and toxicology · 2025Article
- Dexamethasone, celecoxib, and simvastatin-induced 5-fluorouracil resistance in cancer cells: a possible role of lipid droplet accumulation.Discover oncology · 2025Article
- Lipid metabolism involved in progression and drug resistance of breast cancer.Genes & diseases · 2025Review
- Abnormal changes in metabolites caused by mJournal of advanced research · 2025Review
- Lipid metabolic reprogramming drives triglyceride storage and variable sensitivity to FASN inhibition in endocrine-resistant breast cancer cells.Breast cancer research : BCR · 2025Article
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- Article
- Soy Isoflavone Genistein Enhances Tamoxifen Sensitivity in Breast Cancer via microRNA and Glucose Metabolism Modulation.International journal of molecular sciences · 2025Article
- Regulating Lipid MetabolismRecent patents on anti-cancer drug discovery · 2025Article
- Fatty Acid Trafficking Between Lipid Droplets and Mitochondria: An Emerging Perspective.International journal of biological sciences · 2025Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTamoxifen treatment of estrogen receptor (ER)-positive breast cancer reduces mortality by 31%. However, over half of advanced ER-positive breast cancers are intrinsically resistant to tamoxifen and about 40% will acquire the resistance during the treatment.
methodsIn order to explore mechanisms underlying endocrine therapy resistance in breast cancer and to identify new therapeutic opportunities, we created tamoxifen-resistant breast cancer cell lines that represent the luminal A or the luminal B. Gene expression patterns revealed by RNA-sequencing in seven tamoxifen-resistant variants were compared with their isogenic parental cells. We further examined those transcriptomic alterations in a publicly available patient cohort.
resultsWe show that tamoxifen resistance cannot simply be explained by altered expression of individual genes, common mechanism across all resistant variants, or the appearance of new fusion genes. Instead, the resistant cell lines shared altered gene expression patterns associated with cell cycle, protein modification and metabolism, especially with the cholesterol pathway. In the tamoxifen-resistant T-47D cell variants we observed a striking increase of neutral lipids in lipid droplets as well as an accumulation of free cholesterol in the lysosomes. Tamoxifen-resistant cells were also less prone to lysosomal membrane permeabilization (LMP) and not vulnerable to compounds targeting the lipid metabolism. However, the cells were sensitive to disulfiram, LCS-1, and dasatinib.
conclusionAltogether, our findings highlight a major role of LMP prevention in tamoxifen resistance, and suggest novel drug vulnerabilities associated with this phenotype.
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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.