Research Papers:

Association between Retinoic acid receptor-β hypermethylation and NSCLC risk: a meta-analysis and literature review

Yan Li, De-guo Lu, Ying-mei Ma and Hongxiang Liu _

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Oncotarget. 2017; 8:5814-5822. https://doi.org/10.18632/oncotarget.14023

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Yan Li1, De-guo Lu2, Ying-mei Ma2 and Hongxiang Liu3

1 Department of Respiratory, The Ninth People’s Hospital of Chongqing, Chongqing, P. R. China

2 Clinical Laboratory, Linyi People’s Hospital, Linyi, Shandong, P. R. China

3 Department of Cardiothoracic Surgery, Southwest Hospital, Third Military Medical University, Chongqing, P.R. China

Correspondence to:

Hongxiang Liu, email:

Keywords: RARβ, methylation, lung cancer, meta-analysis, tumor suppressor gene

Received: September 06, 2016 Accepted: December 12, 2016 Published: December 19, 2016


Emerging evidence indicates that Retinoic acid receptor-β (RARβ) is a tumor suppressor in many types of tumor. However, whether or not RARβ is a risk factor and is correlated to clinicopathological characteristics of non-small cell lung cancer (NSCLC) remains unclear. In this report, we performed a meta-analysis to determine the effects of RARβ hypermethylation on the incidence of NSCLC and clinicopathological characteristics in human NSCLC patients. Final valuation and analysis of 1780 cancer patients from 16 eligible studies was performed. RARβ hypermethylation was found to be significantly higher in NSCLC than in normal lung tissue, the pooled OR from 7 studies including 646 NSCLC and 580 normal lung tissues, OR = 6.05, 95% CI = 3.56-10.25, p<0.00001. RARβ hypermethylation was significantly higher in adenocarcinoma (AC) compared to squamous cell carcinoma (SCC), pooled OR is 0.68 (95% CI = 0.52-0.89, p = 0.005). RARβ hypermethylation was also found to occur significantly higher in smoker (n = 232) than non-smoker (n = 213) (OR = 2.46, 95% CI = 1.54-3.93, p = 0.0002). Our results indicate that RARβ hypermethylation correlates well with an increased risk in NSCLC patients. RARβ geneinactivation caused by RARβ methylation contributes the NSCLC tumorigenesis and may serve as a potential risk factor, diagnostic marker and drug target of NSCLC.

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