Cancer treatment options are limited due to therapeutic resistance; thus, understanding the tumor microenvironment (TME) is crucial. Sphingolipid metabolism and complement activation products have essential roles in promoting tumor survival. Emerging evidence shows that sphingolipid signaling can regulate intracellular complement activation to induce inflammasome-mediated metastasis, offering a promising strategy for cancer therapy.
Keywords: S1P receptor signaling; complement signaling; sphingolipid metabolism; sphingosine 1-phosphate (S1P).
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