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ABSTRACT: Numerous studies have documented that in cancer therapy flavonoids extracted from traditional Chinese medicine have anti-tumor activity or can enhance efficiency of chemotherapy in combination with chemotherapeutics. Thus, an awareness of flavonoids is needed by physicians and medical researchers. This review provides evidence about anti-hepatocellular carcinoma activity of flavonoids. First, as a common employed in vitro model, profile of HepG2 is shown. Second, the intracellular signaling pathways induced by flavonoids which inhibit the HepG2 cell line are summarized. Third, study situation of anti-HBV/HCV activity of flavonoids is shown. Our review is aimed at providing an understanding of anti-HBV/HCV activity and anti-HCC mechanisms of flavonoids, and an outlook on flavonoids application on cancer therapy.
Drug discoveries & therapeutics. 02/2013; 7(1):1-8.
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Y Minami,
A Abe,
M Minami,
K Kitamura,
J Hiraga,
S Mizuno,
K Ymamoto,
M Sawa, Y Inagaki,
K Miyamura,
T Naoe
Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 03/2012; 26(9):2142-3. · 8.30 Impact Factor
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ABSTRACT: Resistin is an adipocytokine that induces insulin resistance and is predominantly expressed in adipocytes and peripheral blood mononuclear cells. Resistin expression increases in inflammatory diseases as well as diabetes mellitus, and is upregulated by bacterial pathogens and proinflammatory cytokines. The aim of this study was to identify resistin in human gingival crevicular fluid, to compare the resistin levels in gingival crevicular fluid between subjects with and without periodontitis and diabetes mellitus and to investigate the regulation of resistin release from human neutrophils by Porphyromonas gingivalis lipopolysaccharide (P-LPS).
Gingival crevicular fluid samples were collected from patients with chronic periodontitis (n = 24), patients with diabetes mellitus-related periodontitis (n = 18) and healthy subjects (n = 21). Resistin in gingival crevicular fluid was determined using western blot analysis and an ELISA kit. The glycated hemoglobin (HbA(1c)) value was obtained from patients with diabetes mellitus-related periodontitis by a medical interview. Human neutrophils were cultured with P-LPS (0-1000 ng/mL), or incubated with inhibitors of actin or microtubule polymerization in the absence or presence of P-LPS. The medium and cellular fractions were used for determination of resistin by ELISA.
The resistin level in gingival crevicular fluid from patients with periodontitis or diabetes mellitus-related periodontitis was significantly higher than that of healthy subjects. The resistin level in gingival crevicular fluid was correlated with gingival index score, but not blood HbA(1c) value. The P-LPS increased resistin release from human neutrophils, and its induction was decreased by actin polymerization inhibitors.
We show, for the first time, the presence of resistin in gingival crevicular fluid. A high resistin level in gingival crevicular fluid samples from periodontitis patients may to some extent be related to P-LPS-induced resistin release from neutrophils.
Journal of Periodontal Research 02/2012; 47(5):554-62. · 1.69 Impact Factor
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ABSTRACT: c-Met, a type of receptor tyrosine kinase, may be significantly associated with the progression of hepatocellular carcinoma (HCC). In addition, des-γ-carboxyprothrombin (DCP) has been found to interact with c-Met and activate HCC cell growth. Therefore, the functional inhibition of c-Met expressed on HCC cells should arrest HCC cell growth. The present study found that the c-Met inhibitor SU11274 suppressed HCC cell growth by inhibiting the activation of c-Met. Furthermore, this inhibitor also neutralized the activation of HCC cell growth resulting from the addition of DCP. These results suggest that the functional inhibition of c-Met might be a target for the development of chemotherapeutic agents for HCC, and especially those that are positive for expression of DCP.
Bioscience trends 04/2011; 5(2):52-6. · 0.97 Impact Factor
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ABSTRACT: Aberrant expressions of KL-6 mucin were proved to be associated with worse tumor behaviors of many carcinomas. This study was to evaluate the expression KL-6 mucin, a human MUC1 mucin, in intrahepatic cholangiocarcinoma (CC) and its significance in tumor progression.
KL-6 mucin expressions in 21 patients with CC, 12 with combined hepatocellular and cholangiocarcinoma (cHCC-CC), and 78 with hepatocellular carcinoma (HCC) were detected by immunohistochemical staining. The effects of two glycosylation inhibitors (tunicamycin and benzyl-alpha-N-acetylgalactosamine (BAG)) on CC cell proliferations were assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assays. KL-6 mucin expressions were detected by immunocytochemical staining and western blotting after tunicamycin or BAG treatment. Cell adhesive and invasive properties were evaluated by adhesion tests and transwell chamber assays after tunicamycin or BAG treatment.
Positive KL-6 mucin staining was observed in all CC tissues and CC areas of cHCC-CC tissues. Immunocytochemical staining and western blotting showed that KL-6 mucin expressions were significantly reduced after both inhibitors treatment. Cell adhesive properties were significantly decreased after both inhibitors treatment, while cell invasive abilities were significantly decreased after BAG but not tunicamycin treatment.
This study indicated that KL-6 mucin might be a specific tumor target for CC. Therapeutic strategies that target glycosylation of KL-6 mucin may be useful to control aggressive behaviors of CC.
Life sciences 08/2009; 85(9-10):395-400. · 2.56 Impact Factor
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ABSTRACT: KL-6 mucin is a type of MUC1 mucin and its aberrant expression has been shown to be associated with aggressive metastasis and poor clinical outcome in tumors. The present study is to investigate the effects of benzyl-N-acetyl-α-galactosaminide (GalNAc-O-bn), an O-glycosylation inhibitor, on KL-6 mucin expression and invasive properties of a human pancreatic carcinoma cell line, Suit-2 cells. Expression profiles of KL-6 mucin in the cells pretreated with or without 5 mM GalNAc-O-bn for 48 h were examined by Western blotting and immunocytochemical staining and invasive properties were examined by transwell chamber assay. Western blotting and immunocytochemical staining showed that the expression profiles of KL-6 mucin changed significantly after GalNAc-O-bn treatment. Meanwhile, the invasive ability of Suit-2 cells decreased significantly after GalNAc-O-bn treatment (p < 0.05). These results suggest that glycosylation of KL-6 mucin may be closely related to aggressive behaviors of pancreatic cancer cells like metastasis and invasion.
Drug discoveries & therapeutics. 10/2008; 2(5):282-5.
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ABSTRACT: N-myc downstream-regulated gene 1 is detected in normal tissue but is down-regulated in cancer tissue. Furthermore, research has suggested that co-expression with p53 is necessary for induction of p53-mediated apoptosis. This study sought to investigate the clinicopathological significance of N-myc downstream-regulated gene 1 and p53 expression in gastric cancer tissue.
Immunohistochemical detection of N-myc downstream-regulated gene 1 and p53 was performed with tissue samples from 96 cases of gastric cancer, and the relationship between expression profiles of proteins and clinicopathological characteristics was statistically analysed.
Positive staining of N-myc downstream-regulated gene 1 was observed in the cytoplasm (22 of 96 cases, 22.9%) and/or nucleus (29 of 96 cases, 30.2%) of cancer cells. In 15 cases (15.6%), both cytoplasm-positive cells and nucleus-positive cells were observed in the cancerous region. The nuclear localization of N-myc downstream-regulated gene 1 was frequently observed in the region of cancerous invasion and was significantly related to lymph node metastasis. In addition, accumulation of p53 protein in the nucleus of cancer cells significantly coincided with the nuclear localization of N-myc downstream-regulated gene 1.
Localization of N-myc downstream-regulated gene 1 and its significant correlation with p53 expression may play an important role in cancer progression.
Digestive and Liver Disease 08/2008; 41(2):96-103. · 3.05 Impact Factor
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ABSTRACT: AimsAberrant expressions of KL-6 mucin were proved to be associated with worse tumor behaviors of many carcinomas. This study was to evaluate the expression KL-6 mucin, a human MUC1 mucin, in intrahepatic cholangiocarcinoma (CC) and its significance in tumor progression.Main methodsKL-6 mucin expressions in 21 patients with CC, 12 with combined hepatocellular and cholangiocarcinoma (cHCC-CC), and 78 with hepatocellular carcinoma (HCC) were detected by immunohistochemical staining. The effects of two glycosylation inhibitors (tunicamycin and benzyl-alpha-N-acetylgalactosamine (BAG)) on CC cell proliferations were assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assays. KL-6 mucin expressions were detected by immunocytochemical staining and western blotting after tunicamycin or BAG treatment. Cell adhesive and invasive properties were evaluated by adhesion tests and transwell chamber assays after tunicamycin or BAG treatment.Key findingsPositive KL-6 mucin staining was observed in all CC tissues and CC areas of cHCC-CC tissues. Immunocytochemical staining and western blotting showed that KL-6 mucin expressions were significantly reduced after both inhibitors treatment. Cell adhesive properties were significantly decreased after both inhibitors treatment, while cell invasive abilities were significantly decreased after BAG but not tunicamycin treatment.SignificanceThis study indicated that KL-6 mucin might be a specific tumor target for CC. Therapeutic strategies that target glycosylation of KL-6 mucin may be useful to control aggressive behaviors of CC.
Life Sciences.
