ArticleThe Journal of biological chemistry2011
Unfolded protein response is required in nu/nu mice microvasculature for treating breast tumor with tunicamycin.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 105 citations in OpenAlex.
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- Sestrin2 Attenuates Myocardial Endoplasmic Reticulum Stress and Cardiac Dysfunction During Ischemia/Reperfusion Injury.Journal of the American Heart Association · 2024Article
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- Pharmacokinetic Effects of Different Models of Nonalcoholic Fatty Liver Disease in Transgenic Humanized OATP1B Mice.Drug metabolism and disposition: the biological fate of chemicals · 2024Article
- Benefits and Pitfalls of a Glycosylation Inhibitor Tunicamycin in the Therapeutic Implication of Cancers.Cells · 2024Review
- Phosphate availability conditions caspofungin tolerance, capsule attachment and titan cell formation inFrontiers in fungal biology · 2024Article
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- Extracellular arginine availability modulates eIF2α O-GlcNAcylation and heme oxygenase 1 translation for cellular homeostasis.Journal of biomedical science · 2023Article
- BIRTH OF A GLYCOTHERAPY FOR BREAST CANCER.Trends in carbohydrate research · 2023Article
- Deregulation of mTORC1-TFEB axis in human iPSC model ofFrontiers in neuroscience · 2023Article
- SIA-IgG confers poor prognosis and represents a novel therapeutic target in breast cancer.Bioengineered · 2022Article
- Glycotherapy: A New Paradigm in Breast Cancer Research.Biomolecules · 2022Review
- WLS/wntless is essential in controlling dendritic cell homeostasis via a WNT signaling-independent mechanism.Autophagy · 2021Article
- Evaluation of ATAD2 as a Potential Target in Hepatocellular Carcinoma.Journal of gastrointestinal cancer · 2021Article
- Concurrent Evolution of Antiaging Gene Duplications and Cellular Phenotypes in Long-Lived Turtles.Genome biology and evolution · 2021Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Up-regulation of the dolichol pathway, a "hallmark" of asparagine-linked protein glycosylation, enhances angiogenesis in vitro. The dynamic relationship between these two processes is now evaluated with tunicamycin. Capillary endothelial cells treated with tunicamycin were growth inhibited and could not be reversed with exogenous VEGF(165). Inhibition of angiogenesis is supported by down-regulation of (i) phosphorylated VEGFR1 and VEGFR2 receptors; (ii) VEGF(165)-specific phosphotyrosine kinase activity; and (iii) Matrigel(TM) invasion and chemotaxis. In vivo, tunicamycin prevented the vessel development in Matrigel(TM) implants in athymic Balb/c (nu/nu) mice. Immunohistochemical analysis of CD34 (p < 0.001) and CD144 (p < 0.001) exhibited reduced vascularization. A 3.8-fold increased expression of TSP-1, an endogenous angiogenesis inhibitor in Matrigel(TM) implants correlated with that in tunicamycin (32 h)-treated capillary endothelial cells. Intravenous injection of tunicamycin (0.5 mg/kg to 1.0 mg/kg) per week slowed down a double negative (MDA-MB-435) grade III breast adenocarcinoma growth by ∼50-60% in 3 weeks. Histopathological analysis of the paraffin sections indicated significant reduction in vessel size, the microvascular density and tumor mitotic index. Ki-67 and VEGF expression in tumor tissue were also reduced. A significant reduction of N-glycan expression in tumor microvessel was also observed. High expression of GRP-78 in CD144-positive cells supported unfolded protein response-mediated ER stress in tumor microvasculature. ∼65% reduction of a triple negative (MDA-MB-231) breast tumor xenograft in 1 week with tunicamycin (0.25 mg/kg) given orally and the absence of systemic and/or organ failure strongly supported tunicamycin's potential for a powerful glycotherapeutic treatment of breast cancer in the clinic.
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