多環芳香烴類受器與台灣肺癌發生之相關性研究

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學分子毒理學研究所 > 研究計劃 > Item 310902500/3321

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/3321

Title:	多環芳香烴類受器與台灣肺癌發生之相關性研究 Investigating the Role of Aryl Hydrocarbon Receptor in Susceptibility to Lung Cancer in Taiwan
Authors:	林嬪嬪 Lin, Pin-Pin
Contributors:	中山醫學院毒理學研究所
Keywords:	多環芳香烴受器;肺癌;易感性;基因表現 Aryl hydrocarbon receptor (AhR);Lung cancer;Susceptibility;Gene expression
Date:	2002
Issue Date:	2010-12-17T03:05:03Z (UTC)
Abstract:	已知暴露多種空氣中之汙染物與肺癌的發生有關，例如多環芳香烴類，而多環芳香烴類受器(AhR)為多環芳香烴類化合物產生毒性所必須的，因此本計畫目的為探討AhR在台灣地區肺癌易感性所扮演之角色。我們以組織免疫染色檢測肺腫瘤組織中AhR, Arnt, CYP1A1，CYP1B1蛋白表現情形並以ELISA檢測B[a]P DNA鍵結物，以Real-time RT-PCR方法定量肺腫瘤及非腫瘤組織中AhR mRNA。本研究結果顯示AhR, Arnt, CYP1A1, CYP1B1均位於Bronchiolar epithelium及腫瘤細胞，而且AhR，CYP1A1及CYP1B1位於細胞質而Arnt位於細胞核，肺腺癌細胞之AhR, CYP1A1 and CYP1B1免疫染色深度比肺鱗癌細胞深。CYP1B1與AhR免疫染色深淺具相關性，在非吸煙者之肺腺癌中CYP1A1,B[a]P DNA adduct與AhR表現程度具有正相關，而且AhR在肺腺癌中表現比週邊正常上皮細胞高，以Real-time RT-PCR亦發現腫瘤組織AhR mRNA較正常組織高，以研究結果推論，AhR過度表現與非吸煙者之肺腺癌組織中B[a]P DNA adduct形成，CYP1A1-CYP1B1表現有關。最後我們比較肺癌病人與正常人周邊血液中AhR基因表現情形，發現並無顯著差異，因此AhR基因表現並非台灣肺癌發生之易感性因子。而AhR基因在肺腺癌過度表現可能是細胞癌化所造成。 The objective of this project is to evaluate the role of AhR in susceptibility to lung cancer in Taiwan. We have examined AhR, Arnt, CYP1A1 and CYP1B1 expression in human lung-tumor tissues using ˇ之immunohistochemistry method. B[a]P DNA adducts were measured with ELISA. AhR mRNA levels in tumors versus non-tumor tissues were measured with the quantitative real-time RT-PCR assay. AhR, Arnt, CYP1A1 and CYP1B1 were mainly found in the bronchiolar epithelium and neoplasm. AhR, CYP1A1 and Cyp1B1 staining were located in the cytosol, irrespective of Arnt in the nuclei of epithelial cells. AhR, CYP1A1 and CYP1B1 immmunostaining was more intense in adenocarcinoma (AD) than in squamous cell carcinoma (SQ). CYP1B1 levels correlated with AhR levels in lung tumors. CYP1A1 and B[a]P DNA adducts positively correlated with AhR levels in AD of nonsmokers. Furthermore, AhR protein expression was higher in AD than in adjacent bronchial epithelial cells. The increase in AhR expression was also detected at the mRNA levels with the quantitative real-time RT-PCR assay. Our data indicate that AhR was overexpressed in lung AD and suggest that AhR should play a role in B[a]P adduct formation, CYP1A1 and CYP1B1 expression in nonsmokers who developed lung adenocarcinoma. We also compared AhR gene expression in peripheral lymphocytes from lung cancer patients and control subjects with the real-time RT-PCR assay. No significant difference was found between two groups. Therefore, AhR expression was not the susceptibility factor for lung cancer in Taiwan.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/3321
Appears in Collections:	[醫學分子毒理學研究所] 研究計劃

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