Tumor-associated macrophages (TAMs) are a class of immune cells present in the microenvironment of solid tumors.
Though the exact origin of the TAMs is not found, they are known to be highly involved the cancer-related inflammation.
Tumor metastasis which is a major cause of death of cancer patients occurs by the intrinsic alterations in tumor cells and cross-talk between cancer cells and their altered microenvironment components. Tumor-associated macrophages (TAMs) are the key cells that create an immunosuppressive tumor microenvironment (TME) by producing chemokines, cytokines, growth factors, and making the inhibitory immune checkpoint proteins release in T cells.
The composition of macrophages in the tumor microenvironment depends on the type, stage, size, and location of the tumor.
IIT Roorkee Study
In a recent study conducted by a team at IIT Roorkee, Fbln7-C, a C-terminal fragment of the adhesion protein Fibulin7, can delay the reprogramming process of tumor-associated macrophages (TAMs).
As per the study, the protein component can effectively inhibit the proliferation of cancer cells.
The study used an animal breast tumor model and different In vitro systems to point out that Fbln7-C could help the macrophages in resisting the reprogramming process and delaying the process of conversion of anti-tumorigenic to pro-tumorigenic TAMs, while directly inhibiting the rapid increase of cancer cells.
As per the findings of another study, Fbln7-C can regulate the inflammatory functions of human neutrophils. The administration of Fbln7-C can improve survival in animals injected with Lipopolysaccharide (LPS), a cell wall content of gram-negative bacteria.
Initially, Fbln7 was identified in developing tooth and was later shown to be expressed in various other tissues like bone, cartilage, and placenta.
The study was published in the Federation of European Biochemical Societies’ official publication “The FEBS Journal”.