title: Effects of Psoralen as an Anti-tumor Agent in Human Breast Cancer MCF-7/ADR Cells.
abstract: Psoralen is a major active component of Psoralea corylifolia. In the present study, we analyzed psoralen-induced changes in human breast cancer MCF-7/ADR cells and investigated the underlying mechanisms of the anticancer effect on MCF-7/ADR cells. We measured cell viability by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to evaluate the cytotoxicity and multidrug resistance (MDR) reversal activity of psoralen. The cell cycle distribution and apoptosis, accumulation and efflux of rhodamine123 (Rh123), and P-glycoprotein (P-gp) expression levels of MCF-7/ADR cells treated with psoralen were all detected by flow cytometry (FCM). We assessed P-gp ATPase activity by monitoring ATP consumption. We evaluated the activity of nuclear factor-kappaB (NF-κB) and the expression of E-cadherin, vimentin and α-smooth muscle actin (SMA) involved in regulating epithelial-mesenchymal transition (EMT). The results showed that psoralen inhibited the proliferation of MCF-7/ADR cells as shown by G0/G1 phase arrest rather than encouraging apoptosis. It was also observed that psoralen reversed MDR through inhibiting ATPase activity rather than reducing P-gp expression. Our results further showed that psoralen inhibited the migration abilities of MCF-7/ADR cells by repressing EMT possibly through inhibiting the activation of NF-κB. Our findings provided a systematic and detailed description of the anti-cancer effect of psoralen on MCF-7/ADR cells for the exploration of natural compounds as novel anticancer agents.
authors.affiliation: Department of Thyroid and Breast Surgery, The Affiliated Hospital of Binzhou Medical College.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Wang
authors.forename: Kai
authors.initials: K
authors.lastname: Cheng
authors.forename: Yong
authors.initials: Y
authors.lastname: Han
authors.forename: Guoqiang
authors.initials: G
authors.lastname: Zhang
authors.forename: Jianli
authors.initials: J
authors.lastname: Dong
authors.forename: Yuzhen
authors.initials: Y
authors.lastname: Cui
authors.forename: Zhenlin
authors.initials: Z
authors.lastname: Yang
mesh_terms: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000378:metabolism; D000199:Actins / Q000235:genetics; D000251:Adenosine Triphosphatases / Q000378:metabolism; D015703:Antigens, CD; D000970:Antineoplastic Agents / Q000494:pharmacology*; D015820:Cadherins / Q000235:genetics; D002453:Cell Cycle / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D005363:Ficusin / Q000494:pharmacology*; D006801:Humans; D061986:MCF-7 Cells; D016328:NF-kappa B / Q000378:metabolism; D014746:Vimentin / Q000235:genetics
chemical_list: C541116:ACTA2 protein, human; D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D000199:Actins; D015703:Antigens, CD; D000970:Antineoplastic Agents; C513384:CDH1 protein, human; D015820:Cadherins; D016328:NF-kappa B; D014746:Vimentin; D000251:Adenosine Triphosphatases; D005363:Ficusin