title: Silibinin induced the apoptosis of Hep-2 cells via oxidative stress and down-regulating survivin expression.
abstract: Silibinin is an anticancer and chemopreventive natural compound, which is extracted from milk thistle (Silybum marianum). It is reported that silibinin has anticancer efficacy in many malignant tumors. Laryngeal carcinoma is the second most common head and neck squamous carcinoma. In the present work, we investigated the effects of silibinin on laryngeal squamous cell carcinoma (LSCC) cell line Hep-2 cells. We found that silibinin induced the decrease of cell viability in Hep-2 cells with a concentration- and time-dependent manner. Moreover, silibinin resulted in the apoptosis of Hep-2 cells and had synergy effects with arsenic trioxide. Intracellular reactive oxygen species (ROS) accumulation increased because of silibinin exposure. ROS scavenger NAC alleviated the cytotoxicity of silibinin to Hep-2 cells. The mitochondrial membrane potential (MMP) was lost in Hep-2 cells treated with silibinin. Subsequently, silibinin induced the activation of caspase-3 in Hep-2 cells and caspase inhibitor Z-VAD-FMK inhibited the cytotoxicity of silibinin in Hep-2 cells. The survivin expression decreased after Hep-2 cells were treated with silibinin. In conclusion, silibinin induced the apoptosis of Hep-2 cells via oxidative stress and down-regulating survivin expression. Therefore, silibinin is a potential therapeutical agent against LSCC in future.
authors.affiliation: Jining Medical University, Jining, Shandong Province, People's Republic China. yangxinxin1979@yahoo.com.cn
authors.forename: Xinxin
authors.initials: X
authors.lastname: Yang
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Li
authors.forename: Liangxiang
authors.initials: L
authors.lastname: An
authors.forename: Bo
authors.initials: B
authors.lastname: Bai
authors.forename: Jing
authors.initials: J
authors.lastname: Chen
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000032:analysis; D045744:Cell Line, Tumor; D015536:Down-Regulation; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D007822:Laryngeal Neoplasms / Q000378:metabolism / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D009363:Neoplasm Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010087:Oxides / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D017382:Reactive Oxygen Species; D000077385:Silybin; D012838:Silymarin / Q000494:pharmacology*; D000077022:Survivin
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D000975:Antioxidants; D001152:Arsenicals; C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D009363:Neoplasm Proteins; D010087:Oxides; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D012838:Silymarin; D000077022:Survivin; D000077385:Silybin; D053148:Caspase 3; D000077237:Arsenic Trioxide