ArticleInternational journal of cancer2013
Notch3 is activated by chronic hypoxia and contributes to the progression of human prostate cancer.
Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- Effects of genistein supplementation on genome‑wide DNA methylation and gene expression in patients with localized prostate cancer.International journal of oncology · 2017Trial
- Cholesterol-Lowering Treatment Blocks Epithelial-Mesenchymal Transition (EMT) Associated Invasiveness and Drug Resistance in Breast and Colorectal Adenocarcinoma Models.Cancer medicine · 2026Article
- SENP1 drives de novo cholesterogenesis via disrupting SUMOylation-mediated SREBP2-FBXW7 interaction.Cancer & metabolism · 2026Article
- Obesity and prostate cancer - microenvironmental roles of adipose tissue.Nature reviews. Urology · 2023Review
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
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- The lipid rafts in cancer stem cell: a target to eradicate cancer.Stem cell research & therapy · 2022Review
- The association between NOTCH3 expression and the clinical outcome in the urothelial bladder cancer patients.Bosnian journal of basic medical sciences · 2022Article
- SOX8 Knockdown Overcomes Enzalutamide Resistance in Castration-Resistant Prostate Cancer by Inhibiting the Notch Signaling Pathway.BioMed research international · 2022Article
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- Targeting Signaling Pathway Networks in Several Malignant Tumors: Progresses and Challenges.Frontiers in pharmacology · 2021Review
- Mechanistic Insights Delineating the Role of Cholesterol in Epithelial Mesenchymal Transition and Drug Resistance in Cancer.Frontiers in cell and developmental biology · 2021Review
- Role of Cholesterol and Lipid Rafts in Cancer Signaling: A Promising Therapeutic Opportunity?Frontiers in cell and developmental biology · 2021Review
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- The role of cholesterol and cholesterol-driven membrane raft domains in prostate cancer.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- HIF1α-mediated AIMP3 suppression delays stem cell aging via the induction of autophagy.Aging cell · 2019Article
- The clinicopathologic significance of Notch3 expression in prostate cancer.International journal of clinical and experimental pathology · 2019Article
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- The Role ofThe oncologist · 2018Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Prostate cancer (PC) is still the second cause of cancer-related death among men. Although patients with metastatic presentation have an ominous outcome, the vast majority of PCs are diagnosed at an early stage. Nonetheless, even among patients with clinically localized disease the outcome may vary considerably. Other than androgen sensitivity, little is known about which other signaling pathways are deranged in aggressive, localized cancers. The elucidation of such pathways may help to develop innovative therapies aimed at specific molecular targets. We report that in a hormone-sensitive PC cell line, LNCaP, Notch3 was activated by hypoxia and sustained cell proliferation and colony formation in soft agar. Hypoxia also modulated cellular cholesterol content and the number and size of lipid rafts, causing a coalescence of small rafts into bigger clusters; under this experimental condition, Notch3 migrated from the non-raft into the raft compartment where it colocalized with the γ-secretase complex. We also looked at human PC biopsies and found that expression of Notch3 positively correlated with Gleason score and with expression of carbonic anhydrase IX, a marker of hypoxia. In conclusion, hypoxia triggers the activation of Notch3, which, in turn, sustains proliferation of PC cells. Notch3 pathway represents a promising target for adjuvant therapy in patients with PC.
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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.