Galectin-3 (GAL3), which regulates cell proliferation and the function of various immune cell populations, is highly expressed by myeloid and pancreatic cancer cells. However, its role in the pancreatic tumor microenvironment remains unclear.
To provide further insights, researchers led by Yang Chen, Ph.D., generated in vivo models of pancreatic cancer with GAL3 genetically deleted in both cancer and myeloid cells. Deleting GAL3 inhibited pancreatic cancer progression and prolonged survival in these models. Single-cell sequencing revealed that GAL3 deletion enriched antitumor myeloid cells, and it also resulted in upregulation of CXCL12 as a possible compensatory mechanism for cancer progression. Inhibiting both CXCL12 and GAL3 enhanced anti-PD1 immunotherapy treatment response, highlighting the combination’s potential as a therapeutic strategy for patients with pancreatic cancer.