ArticleThe Journal of steroid biochemistry and molecular biology2015
Cross-talk between ER and HER2 regulates c-MYC-mediated glutamine metabolism in aromatase inhibitor resistant breast cancer cells.
Article in The Journal of steroid biochemistry and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 83 citations in OpenAlex.
- Clinical characterization, prognostic, and predictive values of HER2-low in patients with early breast cancer in the PALLAS trial (ABCSG-42/AFT-05/BIG-14-13/PrE0109).Breast cancer research : BCR · 2024Trial
- Evaluating distant recurrence-free survival and location of metastasis in HER2+ breast cancer by ER status.International journal of cancer · 2026Article
- Mitochondrial biology and immune crosstalk in breast cancer: therapeutic opportunities and challenges.Frontiers in immunology · 2026Review
- Landscape of metabolic alterations and treatment strategies in breast cancer.Genes & diseases · 2025Review
- Amino acid metabolism in breast cancer: pathogenic drivers and therapeutic opportunities.Protein & cell · 2025Review
- Lactic acid metabolism: gynecological cancer's Achilles' heel.Discover oncology · 2025Review
- SLC1A5 is a key regulator of glutamine metabolism and a prognostic marker for aggressive luminal breast cancer.Scientific reports · 2025Article
- Transmembrane Amino Acid Transporters in Shaping the Metabolic Profile of Breast Cancer Cell Lines: The Focus on Molecular Biological Subtype.Current issues in molecular biology · 2024Review
- Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024Review
- Article
- Revisiting HER2 in Prostate Cancer from an Inclusive Perspective: From Biomarkers to Omics.Cancers · 2024Review
- Nomograms for predicting recurrence of HER2-positive breast cancer with different HR status based on ultrasound and clinicopathological characteristics.Cancer medicine · 2024Article
- The tRNA Gm18 methyltransferase TARBP1 promotes hepatocellular carcinoma progression via metabolic reprogramming of glutamine.Cell death and differentiation · 2024Article
- Reprogramming of Glutamine Amino Acid Transporters Expression and Prognostic Significance in Hepatocellular Carcinoma.International journal of molecular sciences · 2024Article
- Genomic Alterations of Tumors in HER2-Low Breast Cancers.International journal of molecular sciences · 2024Article
- Estrogen/HER2 receptor crosstalk in breast cancer: combination therapies to improve outcomes for patients with hormone receptor-positive/HER2-positive breast cancer.NPJ breast cancer · 2023Review
- The Metabolic Landscape of Breast Cancer and Its Therapeutic Implications.Molecular diagnosis & therapy · 2023Review
- Deregulated Metabolic Pathways in Ovarian Cancer: Cause and Consequence.Metabolites · 2023Review
- Non-Coding RNAs Modulating Estrogen Signaling and Response to Endocrine Therapy in Breast Cancer.Cancers · 2023Review
- Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Resistance to endocrine therapies in hormone receptor (HR)-positive breast cancer is a significant clinical problem for a considerable number of patients. The oncogenic transcription factor c-MYC (hereafter referred to as MYC), which regulates glutamine metabolism in cancer cells, has been linked to endocrine resistance. We were interested in whether MYC-mediated glutamine metabolism is also associated with aromatase inhibitor (AI) resistant breast cancer. We studied the expression and regulation of MYC and the effects of inhibition of MYC expression in both AI sensitive and resistant breast cancer cells. Considering the role of MYC in glutamine metabolism, we evaluated the contribution of glutamine to the proliferation of AI sensitive and resistant cells, and performed RNA-sequencing to investigate mechanisms of MYC-mediated glutamine utilization in AI resistance. We found that glutamine metabolism was independent of estrogen but still required estrogen receptor (ER) in AI resistant breast cancer cells. The expression of MYC oncogene was up-regulated through the cross-talk between ER and human epidermal growth factor receptor 2 (HER2) in AI resistant breast cancer cells. Moreover, the glutamine transporter solute carrier family (SLC) 1A5 was significantly up-regulated in AI resistant breast cancer cells. ER down-regulator fulvestrant inhibited MYC, SLC1A5, glutaminase (GLS) and glutamine consumption in AI resistant breast cancer cells. Inhibition of MYC, SLC1A5 and GLS decreased AI resistant breast cancer cell proliferation. Our study has uncovered that MYC expression is up-regulated by the cross-talk between ER and HER2 in AI resistant breast cancer cells. MYC-mediated glutamine metabolism is associated with AI resistance of breast cancer.
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