The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia
Liu et al. identify a novel feedforward loop between tumor cells and macrophages that promotes muscle wasting. Specifically, tumor-derived CCL2 activates macrophages to facilitate non-autonomous activation of TWEAK in tumor cells via CCL5/p65 signaling, leading to cachexia. Macrophage depletion and TWEAK inhibition represent promising therapeutic targets for pancreatic cancer cachexia.