Fig. 4.

Schematic illustration of BM therapy medicines in glial cell targeting strategies. A Silibinin downregulates the STAT3 level in astrocytes, thus suppressing the immune effectiveness of metastases support. B The inhibition of the gap junction, which is critical for the metastases-astrocyte crosstalk, although meclofenamate, tonabersat or siRNA is effective in controlling BM. In addition, the construction of nanodelivery platforms such as tailored micelles (T-M/siRNA) have potential for BM therapy. C The mechanism of BM-promoting CSF1R signaling with the CSF2R-STAT5 assistance pathway and the action site of the inhibitors, including PLX3397, BLZ945 and AC4-13. D Tamoxifen and BKM120, which are traditional targeted drugs, exert immunotherapeutic effects by inhibiting the estrogen-STAT3 pathway and PI3K signaling of protumor microglia, respectively. E Diagram of the TLR9 agonist (CpG-C) promoting microglia to clear tumor cells. Created with BioRender.com