ArticleBiochimica et biophysica acta2015
IL4 receptor α mediates enhanced glucose and glutamine metabolism to support breast cancer growth.
Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Amino Acids as Targets for Immunotherapy against Solid Tumors.Cell biochemistry and biophysics · 2026Review
- Loss of IL13RA2 promotes metastatic tumor growth in triple-negative breast cancer via increased AKT and NF-κB signaling.Clinical & experimental metastasis · 2025Article
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- The role of proinflammatory cytokines and CXC chemokines (CXCL1-CXCL16) in the progression of prostate cancer: insights on their therapeutic management.Cellular & molecular biology letters · 2024Review
- Type II Interleukin-4 Receptor Activation in Basal Breast Cancer Cells Promotes Tumor Progression via Metabolic and Epigenetic Modulation.International journal of molecular sciences · 2024Article
- The Tumor Microenvironment: Signal Transduction.Biomolecules · 2024Review
- HUNK as a key regulator of tumor-associated macrophages in triple negative breast cancer.Oncoimmunology · 2024Article
- A Multigene-Panel Study Identifies Single Nucleotide Polymorphisms Associated with Prostate Cancer Risk.International journal of molecular sciences · 2023Article
- Correlation between amino acid metabolism and self-renewal of cancer stem cells: Perspectives in cancer therapy.World journal of stem cells · 2022Review
- Article
- Development and Evaluation of 2-Amino-7-Fluorophenazine 5,10-Dioxide Polymeric Micelles as Antitumoral Agents for 4T1 Breast Cancer.Polymers · 2021Article
- IL-4 and IL-13 Promote Proliferation of Mammary Epithelial Cells through STAT6 and IRS-1.International journal of molecular sciences · 2021Article
- Recruitment of M1 Macrophages May Not Be Critical for Protection against Colitis-Associated Tumorigenesis.International journal of molecular sciences · 2021Article
- Not Only Immune Escape-The Confusing Role of the TRP Metabolic Pathway in Carcinogenesis.Cancers · 2021Review
- Metabolic Codependencies in the Tumor Microenvironment.Cancer discovery · 2021Review
- Therapeutic targeting with DABIL-4 depletes myeloid suppressor cells in 4T1 triple-negative breast cancer model.Molecular oncology · 2021Article
- Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer.International journal of molecular sciences · 2021Review
- Expression of IL4Rα and IL13Rα1 are associated with poor prognosis of soft-tissue sarcoma of the extremities, superficial trunk, and retroperitoneum.Diagnostic pathology · 2021Article
- ASCT2 and LAT1 Contribution to the Hallmarks of Cancer: From a Molecular Perspective to Clinical Translation.Cancers · 2021Review
- The Metabolism Symbiosis Between Pancreatic Cancer and Tumor Microenvironment.Frontiers in oncology · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The type II interleukin-4 receptor (IL4R) is expressed in human breast cancer, and in murine models thereof. It is activated by interleukin-4 (IL4), a cytokine produced predominantly by immune cells. Previously, we showed that expression of IL4Rα, a signaling component of IL4R, mediates enhanced metastatic growth through promotion of tumor cell survival and proliferation. In lymphocytes, these processes are supported by increased glucose and glutamine metabolism, and B lymphocyte survival is dependent upon IL4/IL4R-induced glucose metabolism. However, it is unknown whether IL4R-mediated metabolic reprogramming could support tumor growth. Here, we show that IL4Rα expression increases proliferation thus enhancing primary mammary tumor growth. In vitro, IL4-enhanced glucose consumption and lactate production in 4T1 cells was mediated by IL4Rα. Expression of the glucose transporter GLUT1 increased in response to IL4 in vitro, and enhanced GLUT1 expression was associated with the presence of IL4Rα in 4T1 mammary tumors in vivo. Although IL4 treatment did not induce changes in glucose metabolism in MDA-MB-231 human breast cancer cells, it increased expression of the main glutamine transporter, ASCT2, and enhanced glutamine consumption in both MDA-MB-231 and 4T1 cells. Pharmacologic inhibition of glutamine metabolism with compound 968 blocked IL4/IL4Rα-increased cell number in both cell lines. Our results demonstrate that IL4R mediates enhanced glucose and glutamine metabolism in 4T1 cancer cells, and that IL4-induced growth is supported by IL4/IL4R-enhanced glutamine metabolism in both human and murine mammary cancer cells. This highlights IL4Rα as a possible target for effective breast cancer therapy.
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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.