SIRT1 in B[a]P-induced lung tumorigenesis
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Jianyi Lu1,*, Min Zhang1,*, Zhiyong Huang2,*, Sufang Sun1, Yongliang Zhang1, Lei Zhang1, Lirong Peng1, Ailing Ma1, Pan Ji1, Jia Dai1, Tong Cui1, Heping Liu1, Jimin Gao1
1Zhejiang Provincial Key Laboratory for Technology & Application of Model Organisms, School of Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China
2Department of Cardiothoracic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China
*These authors have contributed equally to this work
Jimin Gao, e-mail: email@example.com
Heping Liu, e-mail: firstname.lastname@example.org
Keywords: B[a]P, SIRT1, TNF-α, β-catenin, lung cancer
Received: February 04, 2015 Accepted: July 16, 2015 Published: July 28, 2015
Benzo[a]pyrene (B[a]P) is a carcinogen in cigarette smoke. We found that B[a]P induced SIRT1 in human bronchial epithelial BEAS-2B cell. SIRT1 was overexpressed in the lung of B[a]P-exposed mice and in human lung cancer biopsies. SIRT1 up-regulated TNF-α and β-catenin and down-regulated the membrane fraction of E-cadherin. In addition, SIRT1 promoted invasion, migration and tumorigenesis of BEAS-2B cells in nude mice upon B[a]P exposure. Thus, SIRT1 is involved in B[a]P-induced transformation associated with activation of the TNF-α/β-catenin axis and is as a potential therapeutic target for lung cancer.
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