Bendamustine combined with rituximab induces pyroptosis to shape an "immunologically hot" tumor microenvironment  in DLBCL cells via the STING pathway
Bendamustine plus rituximab (BR) therapy has demonstrated favorable clinical outcomes in the treatment of DLBCL patients who are intolerant to R-CHOP therapy. In vitro, BR therapy exhibits a synergistic cytotoxic effect on DLBCL cell lines. Mechanistically, BR induces pyroptosis in DLBCL cells by activating the cGAS-STING pathway, leading to the release of inflammatory factors and the formation of an "immunologically hot" microenvironment. Additionally, BR therapy upregulates MHC molecules on the tumor cell surface, thereby augmenting T cell activation and function. Overall design: OCI-LY1 cells were planted in 48-well culture plates and treated in four conditions. B (Bendamustine) group was treated the same as control group for 1 day before exposed to 200uM Bendamustine for 1.5 days. R (Rituximab) group exposed to 10uM Rituximab for 2.5 days. BR (Bendamustine+Rituximab) group exposed to 10uM Rituximab for 1 days before exposed to 200uM Bendamustine and 10uM Rituximab for 1.5 days. The control group was grown in the same culture conditions for 2.5 days without the addition of any drugs.