title: Molecular mechanisms of Lycoris aurea agglutinin-induced apoptosis and G2 /M cell cycle arrest in human lung adenocarcinoma A549 cells, both in vitro and in vivo.
abstract: OBJECTIVE
  Lycoris is aurea agglutinin (LAA) has attracted rising attention due to its remarkable bioactivities. Here, we aimed at investigating its anti-tumor activities.
  
  
  METHODS
  In vitro methods including MTT, cellular morphology observation, FCM and immunoblotting were performed. In vivo methods like detection of tumor volume, body weight and survival ratio, as well as TUNEL staining were performed.
  
  
  CONCLUSIONS
  LAA triggers G2 /M phase cell cycle arrest via up-regulating p21expression as well as down-regulating cdk-1cyclinA singling pathway, and induces apoptotic cell death through inhibiting PI3K-Akt survival pathway in human lung adenocarcinoma A549 cells. While LAA has no significant cytotoxic effect toward normal human embryonic lung fibroblast HELF cells, and moreover, LAA could amplify the antineoplastic effects of cisplatin toward A549 cells. Lastly LAA also bears anti-cancer and apoptosis-inducing effects in vivo, and it could decrease the volume and weight of subcutaneous tumor mass obviously as well as expand lifespan of mice. These findings may provide a new perspective for elucidating the complicated molecular mechanisms of LAA-induced cancer cell growth-inhibition and death, providing a new opportunity of LAA as a potential candidate anti-neoplastic drug for future cancer therapeutics.
authors.affiliation: School of Life Sciences & Key Laboratory of Bio-resources, Ministry of Education, Sichuan University, Chengdu 610064, China.
authors.forename: C-Y
authors.initials: CY
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: H-L
authors.initials: HL
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Shi
authors.forename: N
authors.initials: N
authors.lastname: An
authors.forename: Y-X
authors.initials: YX
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: J-K
authors.initials: JK
authors.lastname: Bao
authors.forename: S-P
authors.initials: SP
authors.lastname: Deng
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D000077192:Adenocarcinoma of Lung; D000373:Agglutinins / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D016203:CDC2 Protein Kinase / Q000096:biosynthesis; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002945:Cisplatin / Q000494:pharmacology; D019925:Cyclin A / Q000096:biosynthesis; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects*; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism*; D031426:Lycoris / Q000378:metabolism*; D008958:Models, Molecular; D062105:Molecular Docking Simulation; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010936:Plant Extracts / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors
chemical_list: D000373:Agglutinins; D000970:Antineoplastic Agents; D019925:Cyclin A; D050759:Cyclin-Dependent Kinase Inhibitor p21; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010936:Plant Extracts; D051057:Proto-Oncogene Proteins c-akt; D016203:CDC2 Protein Kinase; D002945:Cisplatin