title: Apple polysaccharides induce apoptosis in colorectal cancer cells.
abstract: Certain components of apples have been shown to prevent cancer growth and impede cancer progression. We hypothesized that extracted apple polysaccharides (APs) might, therefore, have anticancer effects, through a mechanism involving the induction of apoptosis in cancer cells, partly via the NF-κB pathway. Two human colorectal cancer (CRC) cell lines, HT-29 and SW620, were exposed to different concentrations of APs (0.01, 0.1 or 1 mg/ml). Cell apoptosis was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay by flow cytometry and incorporation of 5'-bromodeoxyuridine (BrdU) into DNA to identify the proliferating cell fraction, using fluorescence microscopy in vitro. The protein levels of NF-κB/p65, I-κBα, pI-κBα, Bax, Bcl-xl and Bcl-2 were evaluated by western blotting. The target sites of APs on CRC cells were assessed by flow cytometry. At concentrations of 0.1 and 1 mg/ml, APs showed apoptosis-inducing effects, increased expressions of Bax, nuclear p65 and cytoplasmic pI-κBα, and decreased expressions of Bcl-2, Bcl-xl and cytoplasmic I-κBα. APs induced apoptosis by slightly activating the NF-κB pathway; the AP target site could be the Toll-like receptor 4 on the cell membrane. These results demonstrate the potential of APs as agents for clinical prevention and treatment of CRC.
authors.affiliation: Department of Pathogen Biology and Immunology, Xi'an Medical                     College, Xi'an 710021, Shaanxi, P.R. China.
authors.forename: Dian
authors.initials: D
authors.lastname: Zhang
authors.forename: Yang
authors.initials: Y
authors.lastname: Sun
authors.forename: Zhenggang
authors.initials: Z
authors.lastname: Yue
authors.forename: Qian
authors.initials: Q
authors.lastname: Li
authors.forename: Jin
authors.initials: J
authors.lastname: Meng
authors.forename: Junajuan
authors.initials: J
authors.lastname: Liu
authors.forename: Xiang
authors.initials: X
authors.lastname: Hekong
authors.forename: Fengliang
authors.initials: F
authors.lastname: Jiang
authors.forename: Man
authors.initials: M
authors.lastname: Mi
authors.forename: Li
authors.initials: L
authors.lastname: Liu
authors.forename: Qibing
authors.initials: Q
authors.lastname: Mei
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D015179:Colorectal Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D020672:I-kappa B Proteins / Q000096:biosynthesis; D027845:Malus / Q000737:chemistry*; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010936:Plant Extracts / Q000494:pharmacology; D011134:Polysaccharides / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D051996:Transcription Factor RelA / Q000096:biosynthesis
chemical_list: D020672:I-kappa B Proteins; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D010936:Plant Extracts; D011134:Polysaccharides; D019253:Proto-Oncogene Proteins c-bcl-2; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha