Angiogenesis is a physiological process in which new blood vessels grow from existing blood vessels. Angiogenesis is the basis of an individual's early development and wound healing, but some cancerous tumors can use the angiogenesis process to promote the growth of their own blood vessels and promote the tumor to change from a benign state to a malignant state.
Now, scientists from institutions such as Genentech and the University of California San Diego have discovered for the first time that a signaling protein involved in the inflammatory response can also enhance tumor resistance during anti-angiogenesis anti-cancer treatment.
As early as the 1980s, researchers worked hard to identify a key gene involved in angiogenesis, VEGF, followed by the development of the first drug to block multiple types of tumors mediated by VEGF (lung, kidney, brain, and colorectal tumors) ) Growth. However, the researchers found that, similar to other therapies, when tumors continue to develop resistance to this VEGF-targeted drug, the effect of the drug becomes worse and worse, which leads to the recurrence of cancer. There is ample evidence that this resistance will be affected by the tumor microenvironment, but the specific mechanism is still unclear.
In this latest study, scientists unveiled a paracrine signaling network between the adaptive immune system and the innate immune system, which is related to the resistance of many types of tumors to VEGF-inhibiting drugs. They focused on the interleukin 17 (IL-17), a member of a family of cytokine signaling molecules involved in the inflammatory response.
The study found that tumor infiltration helper T cells 17 (Th17) and IL-17 induced the expression of granulocyte colony-stimulating factor (G-CSF) through nuclear factor kappa B (NF-κB) and extracellular related kinase (ERK) signals, Immature bone marrow cells were mobilized and recruited into the tumor microenvironment. This signaling effect of IL-17 in (components of the adaptive immune system in the body) tumor infiltrating T cells promotes tumor resistance to VEGF-inhibiting drugs in mouse models.
The researchers pointed out that this research can provide new ideas for the treatment of cancer. If monoclonal antibodies or other inhibitors are used to hinder the action of IL-17, it can potentially promote the clinical efficacy of VEGF-targeted drugs.
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