m6A-Modified BASP1 Regulates IL6 Expression to Induce TAM Infiltration to Promote Gastric Cancer Progression

Gastric cancer (GC) is aggressive with poor prognosis. This study explores m6A's role in BASP1 regulation and its effects on GC via IL6, M2 macrophages, and PI3K/AKT.

This study analyzed GC data from TCGA, used GC cell lines (Hs746T, KATO III, MKN-45, NCI-N87) and nude mice, modulated BASP1 via lentivirus, assessed cell functions with CCK8, wound healing, Transwell, and flow cytometry, investigated m6A's role with MeRIP-PCR and RNA pulldown, and evaluated macrophage polarization and IL6 with co-culture and ELISA. The involvement of the PI3K/AKT signaling pathway was examined using WB and specific inhibitors.

BASP1 is higher in GC tissues and is linked to poor prognosis. Knockdown inhibited cell viability, migration, and invasion and promoted apoptosis. m6A regulated BASP1 via mRNA stability (IGF2BP2 key). BASP1 regulated IL6 via PI3K/AKT, affecting M2 macrophages. Overexpression in vivo accelerated tumor growth and increased M2 macrophages and IL6.

BASP1's role in GC progression and tumor microenvironment modulation via IL6, M2 macrophages, and PI3K/AKT has been elucidated. This provides a basis for new GC therapies targeting BASP1.