Related Experiment Video
Updated: May 7, 2026
09:03
Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
Published on: November 23, 2014
Interleukin-6: an angiogenic target in solid tumours
Kathryn Middleton1, Joanna Jones1, Zarnie Lwin1
1Mater Adult Hospital, Department of Medical Oncology, Raymond Terrace, Brisbane, QLD 4101, Australia.
Critical Reviews in Oncology/Hematology
|September 14, 2013
Summary
Resistance to anti-angiogenic drugs like anti-VEGF antibodies is common. Targeting interleukin-6 (IL-6) may overcome this resistance, improving cancer treatment outcomes.
Area of Science:
- Oncology
- Immunology
Background:
- Anti-angiogenic agents targeting vascular endothelial growth factor (VEGF) have improved survival in various cancers.
- Acquired resistance to anti-VEGF therapy is a significant clinical challenge, leading to disease progression.
Purpose of the Study:
- To review the role of interleukin-6 (IL-6) in tumor angiogenesis and its link to anti-VEGF therapy resistance.
- To explore the potential of anti-IL-6 therapies as a strategy to overcome resistance and improve cancer treatment.
Main Methods:
- Literature review of preclinical and clinical studies on IL-6, VEGF, and anti-angiogenic therapy resistance.
- Analysis of the mechanisms by which IL-6 signaling influences tumor microenvironment and angiogenesis.
Main Results:
- IL-6 signaling promotes pro-angiogenic effects within the tumor microenvironment.
- Elevated IL-6 levels correlate with treatment failure in patients receiving anti-VEGF therapies.
- IL-6 blockade demonstrates potential in preclinical models to enhance anti-angiogenic efficacy.
Conclusions:
- IL-6 is a key mediator in tumor angiogenesis and a driver of resistance to anti-VEGF therapy.
- Targeting IL-6, through anti-IL-6 therapies, represents a promising strategy to enhance response to anti-angiogenic treatments.
- Anti-IL-6 agents could be used in combination with anti-VEGF drugs or as salvage therapy for refractory cancers.
Related Concept Videos
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
02:17The Tumor Microenvironment
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
01:10Mechanism of Angiogenesis
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...