SLC10A3 drives glioblastoma progression by remodeling the immunosuppressive microenvironment and promoting M2 macrophage migration

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SLC10A3 is overexpressed in glioblastoma (GBM) and correlates with poor patient prognosis.
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The study links SLC10A3 to key signaling pathways involved in GBM progression and immune evasion.
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SLC10A3 knockdown reduces GBM cell proliferation, migration, and M2 macrophage recruitment.
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Enhanced crosstalk between SLC10A3-expressing astrocytes and macrophages contributes to immunosuppression.
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SLC10A3 presents a potential therapeutic target for GBM by modulating the tumor microenvironment.

Frontiers In Oncology

by Shuhui Chen, Daogang Qin, Hanyang Lin, Taohui Ding, Wei Liu, Ziqi Yan, Lingting Wang, Bo Kou
May 13, 2026

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