title: [Astaxanthin inhibits proliferation and promotes apoptosis of A549 lung cancer cells via blocking JAK1/STAT3 pathway].
abstract: Objective To investigate the anti-tumor effects of astaxanthin on A549 lung cancer cells and the related mechanisms. Methods A549 cells were cultured with various concentrations of astaxanthin (20, 40, 60, 80, 100 μmol/L), and DMSO at the same concentrations served as vehicle controls. The viability of A549 cells was detected by CCK-8 assay; cell cycle and apoptosis were observed by flow cytometry; and the expressions of B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), signal transducers and activators of transcription 3 (STAT3), and Janus kinase 1 (JAK1) were evaluated by Western blotting. Results CCK-8 assay showed that astaxanthin decreased the proliferation of A549 cells in a dose-dependent manner. Flow cytometry showed that astaxanthin increased the number of cells in the G0/G1 phase and induced apoptosis in A549 cells. Western blotting showed that astaxanthin up-regulated the expression of Bax and down-regulated the expressions of Bcl-2, STAT3 and JAK1. Conclusion Astaxanthin functions as a potent inhibitor of A549 lung cancer cell growth by targeting JAK1/STAT3 signaling pathway.
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
authors.forename: Chuntao
authors.initials: C
authors.lastname: Wu
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
authors.forename: Jinji
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China. *Corresponding author, E-mail: 283233641@qq.com.
authors.forename: Tienan
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
authors.forename: Guimei
authors.initials: G
authors.lastname: Jiao
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
authors.forename: Changzai
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Surgery Oncology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, China.
authors.forename: Baoshan
authors.initials: B
authors.lastname: Hu
mesh_terms: D000072283:A549 Cells; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D015536:Down-Regulation / Q000187:drug effects; D005434:Flow Cytometry; D006801:Humans; D053613:Janus Kinase 1 / Q000378:metabolism*; D008175:Lung Neoplasms / Q000378:metabolism / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D024341:Xanthophylls / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D050796:STAT3 Transcription Factor; D024341:Xanthophylls; D051028:bcl-2-Associated X Protein; C005948:astaxanthine; C507904:JAK1 protein, human; D053613:Janus Kinase 1