Abstract
Malignant glioma is a highly fatal type of brain tumor, and its reoccurrence is largely due to the ordered interactions among the components present in the complex microenvironment. Besides its role in immune surveillance and clearance under physiological conditions, the complement system is expressed in a variety of tumor types and mediates the interactions within the tumor microenvironments. Recent studies have uncovered the broad expression spectrum of complement signaling molecules in the tumor microenvironment and various tumor cells, in particular, malignant glioma cells. Involvement of the complement system in tumor growth, immunosuppression and phenotype transition have also been elucidated. In this review, we enumerate the expression and function of complement molecules in multiple tumor types reported. Moreover, we elaborate the complement pathways in glioma cells and various components of malignant glioma microenvironments. Finally, we summarize the possibility of the complement molecules as prognostic factors and therapeutic targets in the treatment of malignant glioma. Specific targeting of the complement system maybe of great significance and value in the future treatment of multi-type tumors including malignant glioma.
Highlights
Glioblastoma treatments have been largely unsuccessful due to its rapid growth, multidimensional heterogeneity, and stubborn resistance to chemoradiotherapy (Lim et al, 2018)
Unlike early oncology research that focused on the proliferation and invasion of tumor cells, recent studies have shown that almost all solid tumors have a complex but highly ordered tumor microenvironment
Lim et al confirmed that C5a is highly expressed in the Mesenchymal stem-like cells (MSLCs) of glioma microenvironment and promotes a series of malignant behaviors, such as invasion and migration of glioma cells and glioma stem cells (GSCs) through its receptor C5aR1 in vitro and in vivo
Summary
Glioblastoma treatments have been largely unsuccessful due to its rapid growth, multidimensional heterogeneity, and stubborn resistance to chemoradiotherapy (Lim et al, 2018). C3a/C3aR C3a is a small protein secreted originally from C3 cleavage, which can exert its biological functions when combined with its receptor on the surface of target cells through autocrine or paracrine signaling in various tumors (Morgan, 2000).
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