Apigenin potentiates the antitumor activity of 5-FU on solid Ehrlich carcinoma: Crosstalk between apoptotic and JNK-mediated autophagic cell death platforms
Apigenin potentiated 5-FU cytotoxicity in EAC solid tumor models in vivo. It acted via autophagy stimulation, downregulating MCL-1 and Ki-67 expression. It caused JNK activation and ROS accumulation; resulted in tumor growth inhibition. Apigenin can be used as a co-adjuvant agent in cancer therapy.