In vitro, combined therapy inhibited proliferation and enhanced apoptosis through the GPR41 signaling pathway.Enhanced levels of activated DNA fragmentation markers (cleaved caspase-3).Enhanced the expression of TNF-α by downregulating the expression of HDACs and enhancing histone H3 acetylation.In vivo, combined therapy suppressed tumor growth and enhanced histone H3 acetylation and mRNA expression of TNF-α. The gene discussed is CASP3; the disease is neoplasm.