Anti-tumor effect of licochalcone-E is mediated by caspase-dependent apoptosis through extrinsic and intrinsic apoptotic signaling pathways in KB cancer cells
조인아, 강경록, 김수관, 김도경, 김춘성, 이숙영, 조성식, 윤구, 박병수, 김재성,
소속 상세정보
조인아 ( Cho In-A ) - Chosun University Oral Biology Research Institute
강경록 ( Kang Kyeong-Rok ) - Chosun University Oral Biology Research Institute
김수관 ( Kim Su-Gwan ) - Chosun University Oral Biology Research Institute
김도경 ( Kim Do-Kyung ) - Chosun University Oral Biology Research Institute
김춘성 ( Kim Chun-Sung ) - Chosun University Oral Biology Research Institute
이숙영 ( Lee Sook-Young ) - Chosun University Oral Biology Research Institute
조성식 ( Cho Seung-Sik ) - Mokpo National University College of Pharmacy Department of Pharmacy
윤구 ( Yoon Goo ) - Mokpo National University College of Pharmacy Department of Pharmacy
박병수 ( Park Byung-Soo ) - Chosun University Oral Biology Research Institute
김재성 ( Kim Jae-Sung ) - Chosun University Oral Biology Research Institute
Abstract
This study investigates the anti-cancer effects of licochalcone-E (Lico-E), a phenolic chalconoid derived from the genus Glycyrrhiza, in the human KB squamous cancer cell. Concentration-dependent cytotoxicity in KB cells increased following 24 hours of treatment with 12.5, 25, or 50 μg/ml Lico-E, with an estimated IC50 value of approximately 25 μg/ml. Chromatin condensation, a typical apoptotic phenomenon, was observed in KB cells treated with Lico-E. Consistent with this finding, Lico-E increased caspase-3 activity in KB cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was significantly up-regulated by Lico-E treatment. Subsequently, the pro-apoptotic factor caspase-8, a part of the extrinsic apoptotic signaling pathway, was activated in a concentrationdependent manner by Lico-E treatments. Expression of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondriadependent apoptotic signaling pathway, significantly decreased following Lico-E treatment. Conversely, expression of pro-apoptotic factors such as Bax, Bad, Apaf-1, and caspase-9 increased with Lico-E concentrations. Finally, Lico-E activated caspase-3 and Poly (ADP-ribose) polymerase (PARP) to induce cell death. Z-VAD-fmk significantly inhibited cell death through suppression of caspase-3 expression in KB cells treated with Lico-E. Taken together, Lico-E induces KB cell death through death receptor and mitochondriadependent apoptotic signaling pathways.
키워드
Apoptosis;Cancer; Caspases; Chemotherapeutic agent; Licochalcone-E
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