Effects of Epigallocatechin Gallate on modulating M1/M2 macrophages and cancer metastasis in glioblastoma cell line

In this study, the effects of Epigallocatechin Gallate (EGCG) on immunomodulation and epithelial-mesenchymal transition (EMT) in glioblastoma multiforme (GBM) cell lines were comprehensively investigated. It was determined that EGCG inhibited the proliferation of T98G glioblastoma cells in a dose-dependent manner. Additionally, EGCG was found to modulate macrophage phenotypes within the tumor microenvironment, thereby regulating the immune response. Following co-culture of GBM cells with M1 and M2 macrophages, the expression of EMT-related proteins was assessed upon EGCG treatment. These results indicate that EGCG has the potential to shift the immune balance in the tumor microenvironment toward an antitumoral state. Immunocytochemical analyses revealed that EGCG inhibits the epithelial-mesenchymal transition in glioblastoma cells. The increase in E-cadherin expression and the reduction in mesenchymal markers such as N-cadherin and Vimentin suggest that the cells acquire less invasive and metastatic characteristics. These changes support the notion that EGCG significantly reduces the migration and invasion capacity of tumor cells. Furthermore, colony formation assays demonstrated that EGCG markedly decreases the clonal expansion capacity of cancer cells. In conclusion, EGCG not only directly suppresses the proliferation of glioblastoma cells but also exerts antitumoral effects by regulating the function of immune cells within the tumor microenvironment. These findings support the potential use of EGCG as an immunomodulatory agent in glioblastoma therapy and offer promising insights for the development of novel treatment strategies.