title: Pectolinarigenin Suppresses the Tumor Growth in Nasopharyngeal Carcinoma.
abstract: OBJECTIVE
  Nasopharyngeal cancer (NPC) is one of the common human malignant diseases all over the world, and chemotherapy remains the main therapy for NPC. However, the survival and life quality of NPC patients are still very poor. Thus, novel and selective anti-tumor agents are pressingly needed. Our previous study identified pectolinarigenin as a novel effective anti-tumor drug candidate for NPC. In this study, we further investigated its anti-tumor activities and explored the potential molecular mechanism.
  
  
  METHODS
  NPC C666-1 cells were cultured and treated by pectolinarigenin. Cell proliferation assay, colony formation assay, Transwell assay and wound healing assay were conducted and cell apoptosis was detected by flow cytometry. Mitochondrial transmembrane potential and ROS were also observed. NPC subcutaneous xenograft mice model was established to evaluate the anti-tumor effect of pectolinarigenin in vivo.
  
  
  RESULTS
  We observed that treatment of pectolinarigenin inhibited cell viability and cell migration of NPC C666-1 cells in concentration- and time-dependent manner. Pectolinarigenin induced cell apoptosis in C666-1 cells detected by flow cytometry analysis, which was associated with the activation of mitochondrial-related apoptosis and the accumulation of reactive oxygen species (ROS). Pectolinarigenin also activated caspase signaling pathway. The in vivo experiment of subcutaneous xenograft mice model also indicated that the administration of pectolinarigenin could decrease the tumor growth of NPC and no severe toxicity was observed.
  
  
  CONCLUSIONS
  Based on our findings, we conclude that pectolinarigenin could suppress the tumor growth of NPC, which verifies it as a new therapeutic agent for treating this devastating disease.
authors.affiliation: Department of Otolaryngology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
authors.forename: Chengyu
authors.initials: C
authors.lastname: Wang
authors.forename: Yin
authors.initials: Y
authors.lastname: Cheng
authors.forename: Hongyi
authors.initials: H
authors.lastname: Liu
authors.forename: Yaping
authors.initials: Y
authors.lastname: Xu
authors.forename: Hu
authors.initials: H
authors.lastname: Peng
authors.forename: Juntian
authors.initials: J
authors.lastname: Lang
authors.forename: Jianchun
authors.initials: J
authors.lastname: Liao
authors.forename: Haibin
authors.initials: H
authors.lastname: Liu
authors.forename: Huanhai
authors.initials: H
authors.lastname: Liu
authors.forename: Jingping
authors.initials: J
authors.lastname: Fan
mesh_terms: D000818:Animals; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002277:Carcinoma; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002867:Chromones / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008819:Mice, Nude; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000819:agonists / Q000378:metabolism; D015398:Signal Transduction; D047368:Tumor Burden / Q000187:drug effects; D023041:Xenograft Model Antitumor Assays
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D002867:Chromones; D017382:Reactive Oxygen Species; C528671:pectolinarigenin; D020169:Caspases