Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line
碩士 === 國立高雄師範大學 === 生物科技系 === 99 === Cancer is the leading cause of death in recent year. Environmental or occupational carcinogen exposure is closely related to cancer occurrences. It has been reported that overexposure of biphenyl amine compounds contained in smoke and azo-dyes is related to bladd...
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ndltd-TW-099NKNU51110062016-11-10T16:04:46Z http://ndltd.ncl.edu.tw/handle/77493571960956621814 Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line 2-胺基聯苯誘導TSGH-8301膀胱癌細胞株中環氧酵素二型表現的訊息傳遞路徑之探討 Yu-Yang Cheng 鄭宇洋 碩士 國立高雄師範大學 生物科技系 99 Cancer is the leading cause of death in recent year. Environmental or occupational carcinogen exposure is closely related to cancer occurrences. It has been reported that overexposure of biphenyl amine compounds contained in smoke and azo-dyes is related to bladder cancer occurrence. However, the molecular mechanisms of biphenyl amine compounds-induced bladder cancer are still unclear. Many studies have demonstrated that overexpression of cyclooxygenase-2 (COX-2) in neoplastic lesions is associated with carcinogenesis. Whether the biphenyl amine compounds could regulate the expression of COX-2 was investigated in this study. The signaling pathways of biphenyl amine compound-induced COX-2 expression in human bladder cancer cell lines TSGH-8301 cells were further examined. We found that 2-Aminobiphenyl (2-ABP) could induce COX-2 expression in a dose- and time-dependent manner. The reactive oxygen species production (ROS) production, phosphorylation of mitogen-activated protein kinase, ERK and JNK, and activation of transcription factor c-Jun, ATF-2 were enhanced by 2-ABP treatment. Moreover, 2-ABP induced COX-2 expression, ERK/JNK and c-Jun, ATF-2 phosphorylation were significantly inhibited by JNK inhibitor (SP600125) and ERK1/2 inhibitor (U0126). The ROS scavenger, N-acetyl cysteine (NAC), also could attenuate 2-ABP-induced COX-2 expression and c-Jun, ATF-2 phosphorylation. Furthermore, we found that NADPH oxidase inhibitor (apocynin) also has the same inhibitory effects on 2-ABP-induced COX-2 expression and c-Jun, ATF-2 phosphorylation. Stimulation of 2-ABP was also found to induce the expression of NADPH oxidase subunit p22. These results indicated that 2-ABP induces COX-2 expression mediated through NADPH oxidase stimulated ROS production and JNK/ERK activation, which is regulated by transcription factors c-Jun and ATF-2. Chien-Cheng Chen Lei-Chin Chen 陳建成 陳麗琴 2011 學位論文 ; thesis 104 zh-TW |
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碩士 === 國立高雄師範大學 === 生物科技系 === 99 === Cancer is the leading cause of death in recent year. Environmental or occupational carcinogen exposure is closely related to cancer occurrences. It has been reported that overexposure of biphenyl amine compounds contained in smoke and azo-dyes is related to bladder cancer occurrence. However, the molecular mechanisms of biphenyl amine compounds-induced bladder cancer are still unclear. Many studies have demonstrated that overexpression of cyclooxygenase-2 (COX-2) in neoplastic lesions is associated with carcinogenesis. Whether the biphenyl amine compounds could regulate the expression of COX-2 was investigated in this study. The signaling pathways of biphenyl amine compound-induced COX-2 expression in human bladder cancer cell lines TSGH-8301 cells were further examined. We found that 2-Aminobiphenyl (2-ABP) could induce COX-2 expression in a dose- and time-dependent manner. The reactive oxygen species production (ROS) production, phosphorylation of mitogen-activated protein kinase, ERK and JNK, and activation of transcription factor c-Jun, ATF-2 were enhanced by 2-ABP treatment. Moreover, 2-ABP induced COX-2 expression, ERK/JNK and c-Jun, ATF-2 phosphorylation were significantly inhibited by JNK inhibitor (SP600125) and ERK1/2 inhibitor (U0126). The ROS scavenger, N-acetyl cysteine (NAC), also could attenuate 2-ABP-induced COX-2 expression and c-Jun, ATF-2 phosphorylation. Furthermore, we found that NADPH oxidase inhibitor (apocynin) also has the same inhibitory effects on 2-ABP-induced COX-2 expression and c-Jun, ATF-2 phosphorylation. Stimulation of 2-ABP was also found to induce the expression of NADPH oxidase subunit p22. These results indicated that 2-ABP induces COX-2 expression mediated through NADPH oxidase stimulated ROS production and JNK/ERK activation, which is regulated by transcription factors c-Jun and ATF-2.
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author2 |
Chien-Cheng Chen |
author_facet |
Chien-Cheng Chen Yu-Yang Cheng 鄭宇洋 |
author |
Yu-Yang Cheng 鄭宇洋 |
spellingShingle |
Yu-Yang Cheng 鄭宇洋 Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
author_sort |
Yu-Yang Cheng |
title |
Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
title_short |
Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
title_full |
Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
title_fullStr |
Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
title_full_unstemmed |
Signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in TSGH-8301 bladder cancer cell line |
title_sort |
signaling transduction pathways involved in 2-aminobiphenyl regulating cyclooxygenase-2 expression in tsgh-8301 bladder cancer cell line |
publishDate |
2011 |
url |
http://ndltd.ncl.edu.tw/handle/77493571960956621814 |
work_keys_str_mv |
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