<i>Ganoderma microsporum</i> Immunomodulatory Protein (GMI) Enhances Phagocytosis by Suppressing STAT3/CD47 Signaling in EGFR-Mutant NSCLC Resistant to Gefitinib and Osimertinib.
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ABSTRACT: Target therapy is effective for epidermal growth factor receptor (EGFR) mutation in non-small cell lung cancer (NSCLC). However, resistance often occurs after treatment for several months. Macrophages have difficulty in devouring resistant cells. Ganoderma immunomodulatory protein (GMI) exhibits anti-tumour and immunomodulatory activities. This study aimed to investigate whether GMI overcomes Osimertinib (Tagrisso) and Gefitinib (Iressa) resistance via enhancing macrophage polarization. GMI attenuated signal transducer and activator of transcription 3 (STAT3) phosphorylation and downstream CD47 expression in parental and resistant cells via Western blot and RT-qPCR. Overexpressed STAT3 restored GMI-induced apoptosis and GMI-reduced transcription of CD47 in HCC827 and H1975 lung canc
SUBMITTER: Hsieh YC
PROVIDER: S-EPMC12719595 | biostudies-literature | 2026
REPOSITORIES: biostudies-literature
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