Specific long non-coding RNAs response to occupational PAHs exposure in coke oven workers

Chen Gao; Zhini He; Jie Li; Xiao Li; Qing Bai; Zhengbao Zhang; Xiao Zhang; Shan Wang; Xinhua Xiao; Fangping Wang; Yan Yan; Daochuan Li; Liping Chen; Xiaowen Zeng; Yongmei Xiao; Guanghui Dong; Yuxin Zheng; Qing Wang; Wen Chen

doi:10.1016/j.toxrep.2015.12.011

Specific long non-coding RNAs response to occupational PAHs exposure in coke oven workers

Toxicol Rep. 2016 Jan 4:3:160-166. doi: 10.1016/j.toxrep.2015.12.011. eCollection 2016.

Authors

Chen Gao¹, Zhini He¹, Jie Li¹, Xiao Li¹, Qing Bai¹, Zhengbao Zhang¹, Xiao Zhang², Shan Wang¹, Xinhua Xiao¹, Fangping Wang¹, Yan Yan³, Daochuan Li¹, Liping Chen¹, Xiaowen Zeng¹, Yongmei Xiao¹, Guanghui Dong¹, Yuxin Zheng², Qing Wang¹, Wen Chen¹

Affiliations

¹ Guangzhou Key Laboratory of Environmental Pollution and Health Risk Assessment, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, China.
² Key Laboratory of Chemical Safety and Health, National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
³ Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, China.

Abstract

To explore whether the alteration of lncRNA expression is correlated with polycyclic aromatic hydrocarbons (PAHs) exposure and DNA damage, we examined PAHs external and internal exposure, DNA damage and lncRNAs (HOTAIR, MALAT1, TUG1 and GAS5) expression in peripheral blood lymphocytes (PBLCs) of 150 male coke oven workers and 60 non-PAHs exposure workers. We found the expression of HOTAIR, MALAT1, and TUG1 were enhanced in PBLCs of coke oven workers and positively correlated with the levels of external PAHs exposure (adjusted P_trend < 0.001 for HOTAIR and MALAT1, adjusted P_trend = 0.006 for TUG1). However, only HOTAIR and MALAT1 were significantly associated with the level of internal PAHs exposure (urinary 1-hydroxypyrene) with adjusted β = 0.298, P = 0.024 for HOTAIR and β = 0.090, P = 0.034 for MALAT1. In addition, the degree of DNA damage was positively associated with MALAT1 and HOTAIR expression in PBLCs of all subjects (adjusted β = 0.024, P = 0.002 for HOTAIR and β = 0.007, P = 0.003 for MALAT1). Moreover, we revealed that the global histone 3 lysine 27 trimethylation (H3K27me3) modification was positively associated with the degree of genetic damage (β = 0.061, P < 0.001) and the increase of HOTAIR expression (β = 0.385, P = 0.018). Taken together, our findings suggest that altered HOTAIR and MALAT1 expression might be involved in response to PAHs-induced DNA damage.

Keywords: 1-OHP, 1-hydroxypyrene; 1-hydroxypyrene (PubChem CID: 21387); DNA damage response; GAS5, growth arrest-specific 5; H2K27me3, histone 3 lysine 27 trimethylation; HOTAIR; HOTAIR, HOX transcript antisense RNA; Long non-coding RNA; MALAT; MALAT1, metastasis-associated lung adenocarcinoma transcript 1; PAHs, polycyclic aromatic hydrocarbons; PBLCs, peripheral blood lymphocytes; Peripheral blood lymphocytes; Polycyclic aromatic hydrocarbons; TUG1, taurine up-regulated 1; lncRNAs, long non-coding RNAs.