title: Pu-erh tea inhibits tumor cell growth by down-regulating mutant p53.
abstract: Pu-erh tea is a kind of fermented tea with the incorporation of microorganisms' metabolites. Unlike green tea, the chemical characteristics and bioactivities of Pu-erh tea are still not well understood. Using water extracts of Pu-erh tea, we analyzed the tumor cell growth inhibition activities on several genetically engineered mouse tumor cell lines. We found that at the concentration that did not affect wild type mouse embryo fibroblasts (MEFs) growth, Pu-erh tea extracts could inhibit tumor cell growth by down-regulated S phase and cause G1 or G2 arrest. Further study showed that Pu-erh tea extracts down-regulated the expression of mutant p53 in tumor cells at the protein level as well as mRNA level. The same concentration of Pu-erh tea solution did not cause p53 stabilization or activation of its downstream pathways in wild type cells. We also found that Pu-erh tea treatment could slightly down-regulate both HSP70 and HSP90 protein levels in tumor cells. These data revealed the action of Pu-erh tea on tumor cells and provided the possible mechanism for Pu-erh tea action, which explained its selectivity in inhibiting tumor cells without affecting wild type cells. Our data sheds light on the application of Pu-erh tea as an anti-tumor agent with low side effects.
authors.affiliation: Lab of Molecular Genetics of Aging & Tumor, Faculty of Life Science and Technology, Kunming University of Science & Technology, Kunming 650224, Yunnan, China; E-Mails:  zlj_nwu@163.com  (L.Z.);  lilith-jia@hotmail.com  (S.J.);  twr@sina.com  (W.T.).
authors.forename: Lanjun
authors.initials: L
authors.lastname: Zhao
authors.forename: Shuting
authors.initials: S
authors.lastname: Jia
authors.forename: Wenru
authors.initials: W
authors.lastname: Tang
authors.forename: Jun
authors.initials: J
authors.lastname: Sheng
authors.forename: Ying
authors.initials: Y
authors.lastname: Luo
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D015536:Down-Regulation; D005285:Fermentation; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects; D050884:HSP72 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D018841:HSP90 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D050505:Mutant Proteins / Q000235:genetics / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016196:S Phase / Q000187:drug effects; D013662:Tea / Q000737:chemistry*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D050884:HSP72 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; D050505:Mutant Proteins; D010936:Plant Extracts; D012333:RNA, Messenger; D013662:Tea; D016159:Tumor Suppressor Protein p53