The Effect of Celecoxib on Hepatocellular Carcinoma
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The Effect of Celecoxib on Hepatocellular Carcinoma

The Effect of Celecoxib on Hepatocellular Carcinoma


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About the Book

This dissertation, "The Effect of Celecoxib on Hepatocellular Carcinoma" by Chi-man, Terence, Tang, 鄧致文, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled The effect of celecoxib on hepatocellular carcinoma Submitted by Terence Tang Chi Man For the degree of Doctor of Philosophy at the University of Hong Kong in August 2005 Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in males in Hong Kong in the year of 2004. Previous studies have shown increased levels of cyclooxygenase-2 (COX-2) in a variety of human malignancies including HCC, suggesting that abnormal COX-2 expression plays an important role in carcinogenesis. In addition, some evidence suggests that selective COX-2 inhibitors suppress the formation of tumors in experimental models. However, the significance of COX-2 in progression of HCC remains unclear, and there are no data in the literature on the use of COX-2 inhibitor in HCC. The main objectives of this project were to evaluate the role of COX-2 in human HCC, and to investigate the in vitro and in vivo effects of celecoxib on HCC. Firstly, we evaluated the significance of COX-2 in HCC by examining the relationship between COX-2 and VEGF 165 levels and clinicopathological features. This study showed that elevated COX-2 levels correlated with elevated VEGF levels and invasiveness in HCC. Our data suggested that COX-2 plays a significant role in the invasiveness of HCC, possibly via its angiogenic effect. viSecondly, we performed in vivo studies to investigate the chemopreventive and therapeutic effects of celecoxib, a selective COX-2 inhibitor, on the development and growth of HCC xenograft in nude mice. Our results showed that celecoxib could prolong the latent period of HCC xenograft development in nude mice and decreased the growth of established HCC xenograft in nude mice significantly. However, there was no significant decrease in MVD and VEGF level in the treatment groups compared with the control groups. In in vitro studies, celecoxib induced apoptosis significantly in HCC cell lines and HUVEC. Interestingly, celecoxib induced G1 arrest in both HCC cell lines but not in HUVEC. We have found that the cyclin D1 decreased as the concentration of celecoxib increased. Celecoxib most likely induced apoptosis through the down-regulation of phosphorylation of NFκB, which reduced the cyclin D1 expression, and hence inhibition of proliferation in celecoxib-treated xenografts and cell lines. Finally, we investigated the gene profiling of celecoxib and COX-2 modulation in HCC in the in vitro study by oligo microarray analysis. We aimed to investigate the COX-2-dependent and -independent pathways caused by celecoxib treatment in HCC. Our microarray data suggested that celecoxib may act on both COX-dependent and -independent pathways. We verified six genes by using RT- PCR and northern blot analysis from our microarray data. Three genes (RRM2, KNG1, and FABP1) from COX-2-dependent pathways and three genes (ATF3, CXCL5, and SERPINC1) from COX-independent pathways were considered worthy of further study. In conclusion, our data suggest that COX-2 expression is significantly associated with progression of HCC, and the selective COX-2 inhibitor, celecoxib, can delay the development of HCC and suppress the growth of established HCC in vii experimental animals, most likely via the growth arrest and apoptosis pathways. COX-2 inhibition appears to be a promising strategy for chemoprevention and treatment of HCC


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Product Details
  • ISBN-13: 9781361237717
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 234
  • Weight: 830 gr
  • ISBN-10: 1361237716
  • Publisher Date: 26 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 14 mm
  • Width: 216 mm


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