Volume 5, Issue 3
Clinical Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China
Published：30 September 2025
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Liu Yuxuan.EGFR Expression and Mechanism of Action in Glioblastoma[J].Biomedical Data Science,2025,05(03):110-114.
Liu Yuxuan.EGFR Expression and Mechanism of Action in Glioblastoma[J].Biomedical Data Science,2025,05(03):110-114. DOI： 10.47297/wspbdsWSP2752-630522.20250503.
Epidermal growth factor receptor (EGFR) is frequently abnormal in about 60% of glioblastoma (GBM) patients
mainly manifested by gene amplification and EGFRvIII mutation
resulting in continuous activation of downstream signaling pathways
driving tumor cell proliferation
invasion
migration and stem cell characteristics maintenance. Multiple factors influence these pathways by regulating EGFR activity and stability through different mechanisms. In tumor microenvironment
secreted protein POSTN inhibits EGFR degradation
inflammatory factor PTX3 activates PI3K pathway
and JAK2/STAT3/STAT6 pathway induces M2-type macrophage polarization
which jointly promote GBM progression. In addition
EGFR signaling promotes tumor stem cells to differentiate into endothelial-like cells through RTK/PI3K/AKT pathway
forming vascular mimicry (VM) and accelerating tumor invasion and metastasis. Therapeutic strategies targeting EGFR include monoclonal antibodies and small molecule tyrosine kinase inhibitors
but have limited efficacy and resistance;CAR-T cell therapy targeting EGFR faces challenges such as tumor microenvironment inhibition. So further understanding of EGFR regulatory networks and drug resistance mechanisms is essential to optimize GBM therapy.
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