Oncogenic Function of Twist in the Development and Progression of Prostate Cancer
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Home > Medicine & Health Science textbooks > Pre-clinical medicine: basic sciences > Anatomy > Oncogenic Function of Twist in the Development and Progression of Prostate Cancer
Oncogenic Function of Twist in the Development and Progression of Prostate Cancer

Oncogenic Function of Twist in the Development and Progression of Prostate Cancer


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About the Book

This dissertation, "Oncogenic Function of TWIST in the Development and Progression of Prostate Cancer" by Wai-kei, Kwok, 郭慧琪, 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 Oncogenic function of TWIST in the development and progression of prostate cancer Submitted by Kwok Wai Kei for the degree of Doctor of Philosophy at The University of Hong Kong in August 2007 Prostate cancer is one of serious health problems in the world and currently androgen ablation therapy is the most effective treatment in controlling the growth of tumor, however, hormone refractory prostate cancer is always developed in patients. Better understanding of the underlying molecular mechanisms responsible for prostate carcinogenesis may provide insights for the development of novel therapeutic approaches. TWIST is a basic helix-loop-helix transcription factor that is crucial for mesodermal development during embryogenesis. Recent studies have suggested TWIST as a potential oncogene that is able to promote malignant transformation, increase resistance to chemotherapeutic treatment and induce cancer metastasis. In addition, an immunohistochemistry study has demonstrated that TWIST expression is elevated in prostate cancer tissue specimens when compared with non-malignant tissues, suggesting TWIST may contribute to the development of prostate cancer. However, the role of TWIST during development and progression of prostate cancer is still not known. Thus, the aim of first part of my study was to study the role of TWIST on survival and metastatic ability of prostate cancer cells and to investigate the molecular mechanisms responsible for its action. Using two androgen-independent prostate cancer cell lines, DU145 and PC-3 and one androgen-dependent prostate cancer cell line, LNCap, I found that TWIST inactivation in DU145 and PC-3 resulted in increased sensitivity to a commonly used anti-cancer drug, taxol, which was associated with decreased Bcl-2/Bax ratio and activation of p53-independent apoptosis. In addition, I also showed that ectopic TWIST expression could promote epithelial mesenchymal transition (EMT) in androgen-dependent prostate cancer cells which was accompanied with the suppression of E-cadherin and increased invasion and migration ability of cancer cells. And TWIST inactivation on the other hand could reverse-EMT and suppress invasion in androgen-independent prostate cancer cells. Thus, all these lines of evidence suggest that TWIST is a key factor in prostate cancer cell growth and is a potential therapeutic target to inhibit the growth and metastasis of androgen-independent prostate cancer. In addition to its positive role in cancer development, recently, TWIST was shown to promote anchorage-independent growth in mouse cells and its overexpression was able to protect mouse fibroblasts from anti-cancer drug induced apoptosis, suggesting its expression may be able to provide survival advantage in non-malignant prostate epithelial (PrEC) cells. Therefore, the aim of the second part of my study was to investigate the effect of TWIST on the growth of PrEC cells. To achieve this aim, TWIST expression was altered in two PrEC cell lines, NPTX and HPr-1. I found that overexpression of TWIST in these two cell lines suppressed ARF cellular senescence which was associated with downregulation of p14 as well as ARF inhibition of p14 mediated DNA damage response pathways, MDM2/p53 and Chk1/2 signaling in response to genotoxic stress. These results demonstrated that TWIST expression is essential for overcoming cellular senescence in non-malignant epithelial


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Product Details
  • ISBN-13: 9781361420690
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 232
  • Weight: 830 gr
  • ISBN-10: 1361420693
  • Publisher Date: 27 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 14 mm
  • Width: 216 mm


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