title: Licochalcone B Arrests Cell Cycle Progression and Induces Apoptosis in Human Breast Cancer MCF-7 Cells.
abstract: BACKGROUND
  Recent patent of licochalcone B (LCB) as an antiinflammatory agent has been developed. Emerging evidence shows that LCB may be a promising alternative compound with anti-cancer activities. However, the anticancer mechanism of LCB in MCF-7 cells has not been fully investigated.
  
  
  OBJECTIVE
  We aimed to unearth the anti-cancer effect and mechanism of LCB in MCF-7 cells.
  
  
  METHODS
  Cell proliferation activity and cell-cycle progression were determined by sulforhodamine B assay and flow cytometry, respectively. The mRNA and protein levels of cell cycle-related proteins and apoptosis-associated proteins were examined by RT-qPCR and western blot, respectively. Mitochondrial membrane potential (MMP) was measured by flow cytometry after JC-1 staining.
  
  
  RESULTS
  We found that LCB inhibited MCF-7 cells proliferation in a concentration- and time-dependent manner. Moreover, LCB-treatment led to S phase arrest in MCF-7 cells, which could be elucidated by the decreased mRNA and protein levels of Cyclin A, Cdk2 and Cdc25 A, and the increased protein level of p21. LCB also induced such apoptosis morphology as phosphatidylserine externalization, chromatin condensation and DNA fragmentation. Moreover, LCB led to the loss of MMP, resulting in the release of cytochrome C. The above apoptotic events were supported by the fact that LCB upregulated the mRNA and protein levels of Caspase 3, Caspase 9 and Bax, and downregulated the mRNA and protein level of Bcl-2, which was triggered by the increased p53 protein level in LCB-treated MCF-7 cells.
  
  
  CONCLUSIONS
  These findings suggested that LCB could be a promising agent for treatment of human breast cancer.
authors.forename: Lina
authors.initials: L
authors.lastname: Yu
authors.forename: Jun
authors.initials: J
authors.lastname: Ma
authors.forename: Jichun
authors.initials: J
authors.lastname: Han
authors.forename: Bo
authors.initials: B
authors.lastname: Wang
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Chen
authors.forename: Caixia
authors.initials: C
authors.lastname: Gao
authors.forename: Defang
authors.initials: D
authors.lastname: Li
authors.affiliation: Binzhou Medical University, Yantai 264003, P.R. China. zqsyt@sohu.com.
authors.forename: Qiusheng
authors.initials: Q
authors.lastname: Zheng
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018797:Cell Cycle Proteins / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D047188:Chalcones / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D061986:MCF-7 Cells; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D059807:S Phase Cell Cycle Checkpoints / Q000187:drug effects*; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D051017:Apoptosis Regulatory Proteins; D018797:Cell Cycle Proteins; D047188:Chalcones; C541528:licochalcone B