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Articles by R Pang
Total Records ( 2 ) for R Pang
  Y Dai , L Qiao , K. W Chan , M Yang , J Ye , J Ma , B Zou , Q Gu , J Wang , R Pang , H.Y Lan and B. C.Y. Wong
 

Down-regulation of XIAP (X-linked inhibitor of apoptosis protein) sensitizes colon cancer cells to the anticancer effect of peroxisome proliferator-activated receptor- (PPAR) ligands in mice. The aims of this study were to evaluate the effect of embelin (2,5-dihydroxy-3-undecyl-1,4-benzoquinone), an antagonist of XIAP, on colon cancer, with a particular focus on whether PPAR is required for embelin to exert its effect. A dominant-negative PPAR was used to antagonize endogenous PPAR in HCT116 cells. Cells were treated with or without embelin. Cell proliferation, apoptosis, and nuclear factor-B (NF-B) activity were measured. For in vivo studies, 1,2-dimethylhydrazine dihydrochloride (DMH) was s.c. injected to induce colon cancer in PPAR+/+ and PPAR+/– mice. Mice were fed embelin daily for 10 days before DMH injection, and continued for 30 more weeks. Embelin inhibited proliferation and induced apoptosis in HCT116 cells with marked up-regulation of PPAR. In addition, embelin significantly inhibited the expressions of survivin, cyclin D1, and c-Myc. These effects were partially dependent on PPAR. PPAR+/– mice were more susceptible to DMH-induced colon carcinogenesis than PPAR+/+ mice, and embelin significantly reduced the incidence of colon cancer in PPAR+/+ mice but not in PPAR+/– mice. Embelin inhibited NF-B activity in PPAR+/+ mice but marginally so in PPAR+/– mice. Thus, reduced expression of PPAR significantly sensitizes colonic tissues to the carcinogenic effect of DMH. Embelin inhibits chemical carcinogen-induced colon carcinogenesis, but this effect is partially dependent on the presence of functional PPAR, indicating that PPAR is a necessary signaling pathway involved in the antitumor activity of normal organisms. [Cancer Res 2009;69(11):4776–83]

  W Zhang , B Jiang , Z Guo , C Sardet , B Zou , C. S. C Lam , J Li , M He , H. Y Lan , R Pang , I. F. N Hung , V. P. Y Tan , J Wang and B. C. Y. Wong
 

Background and Aims: Cancer invasion and metastasis may associate with the phenotype transition called epithelial-mesenchymal transition (EMT). We aim to evaluate the impact of four-and-a-half LIM protein 2 (FHL2) on EMT and invasion of colon cancer. Methods: The functional role of FHL2 in EMT was determined by overexpression or small interfering RNA-mediated depletion of FHL2. Mechanisms of FHL2 on expression or activity of E-cadherin and β-catenin were assessed. Results: FHL2 was highly expressed in primary and metastatic colon cancer but not in normal tissues. FHL2 was critical for cancer cell adhesion to extracellular matrix, migration and invasion. FHL2 expression was stimulated by transforming growth factor (TGF)-β1. Moreover, FHL2 acted as a potent EMT inducer by stimulating vimentin and matrix metalloproteinase-9 expressions and causing a loss of E-cadherin, whereas those alterations of EMT markers were not affected by silencing of Smad molecules (typical TGF-β signal mediators) in FHL2 stable transfectant cells. Therefore, FHL2 induced EMT in a TGF-β-dependent and Smad-independent manner. FHL2 downregulated E-cadherin expression and inhibited the formation of membrane-associated E-cadherin–β-catenin complex. FHL2 also stabilized nuclear β-catenin, resulting in enforcement of β-catenin transactivation activity. Conclusion: FHL2 is a potent EMT inducer and might be an important mediator for invasion and/or metastasis of colon cancer.

 
 
 
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