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This dissertation, "Anti-tumor Mechanisms of Cyclooxygenase Inhibitors and a C-Jun-N-terminal Kinase Inhibitor in Gastrointestinal Cancers" by Hua, He,, 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 Anti-Tumor Mechanisms of Cyclooxygenase Inhibitors and a c-Jun-N-Terminal Kinase Inhibitor in Gastrointestinal Cancers Submitted by Hua He for the degree of Master of Philosophy at the University of Hong Kong in August, 2004 We assessed the anti-tumor effect and the mechanisms of cyclooxygenase inhibitors and a c-Jun-N-terminal kinase inhibitor in gastric and colon cancers. In the first study, we investigated whether the anti-tumor effect of cyclooxygenase inhibitors, also known as non-steroidal anti-inflammatory drugs (NSAIDs), is related to telomerase activity. Telomerase activation is observed in most human cancers, and plays an important role in carcinogenesis. Human telomerase reverse transcriptase (hTERT) is a subunit of telomerase that is essential for telomerase activity. PCR-based TRAP-ELISA assay was used to measure the telomerase activity in gastric and colon cancer cell lines after treatment with aspirin, indomethacin, or a specific cyclooxygenase-2 (COX-2) inhibitor, SC-236. SC-236 significantly inhibited telomerase activity in HT-29, COLO205 and CRL-2134 colon cancer cell lines but not in AGS and SW1116 cell lines. The inhibition was COX-2 independent. Similarly, SC- 236 inhibited hTERT mRNA expression in COLO205 and HT-29 cell lines and protein expression in COLO205 cell but not in HT-29, AGS and SW1116 cells. No inhibitory effect on the hTERT transc