Silibinin induces oral cancer cell apoptosis and reactive oxygen species generation by activating the JNK/c-Jun pathway
Haibo Zhang, Hyeon-Jin Kim, Siyong Kim, Hai Huang, Eun-Kyung Kim, Lei Ma, Dong‐Wook Kim, Chae Yeon Kim, Kanghyun Park, Sijun Park, Jiwon Ko, Eun‐Kyong Kim, Ki‐Rim Kim, Zae Young Ryoo, Junkoo Yi, Myoung Ok Kim
Abstract
arrest, ROS generation, and activation of the JNK/c-Jun pathway. Importantly, silibinin effectively suppressed xenograft tumor growth in nude mice. Our findings indicate that silibinin may be a promising option for the prevention or treatment of oral cancer.
Topics & Concepts
SilibininApoptosisCancer researchCell cycleReactive oxygen speciesCancer cellCancerIn vivoCell growthChemistryBiologyPharmacologyMedicineCell biologyBiochemistryInternal medicineBiotechnologySilymarin and Mushroom PoisoningVenomous Animal Envenomation and StudiesFlavonoids in Medical Research