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The methylation profiles of PRDM promoters in non–small cell lung cancer

Authors Tan SX, Hu RC, Xia Q, Tan YL, Liu JJ, Gan GX, Wang LL

Received 11 November 2017

Accepted for publication 25 March 2018

Published 22 May 2018 Volume 2018:11 Pages 2991—3002

DOI https://doi.org/10.2147/OTT.S156775

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 4

Editor who approved publication: Dr Jianmin Xu


Shuang-xiang Tan,1,2 Rui-cheng Hu,1,2 Qian Xia,2 Yong-li Tan,1 Jing-jing Liu,1 Gui-xiang Gan,1 Li-le Wang1

1Hunan Province Institute of Gerontology, Hunan Provincial People’s Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, China; 2Department of Respiratory Medicine, Hunan Provincial People’s Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, China

Background: Non–small cell lung cancer (NSCLC) is one of the leading malignant tumors worldwide. Aberrant gene promoter methylation contributes to NSCLC, and PRDM is a tumor suppressor gene family that possesses histone methyltransferase activity. This study aimed to investigate whether aberrant methylation of PRDM promoter is involved in NSCLC.
Materials and methods: Primary tumor tissues, adjacent nontumorous tissues, and distant lung tissues were collected from 75 NSCLC patients including 52 lung squamous cell carcinoma (LSCC) patients and 23 lung adenocarcinoma patients. The expression of PRDMs was detected by polymerase chain reaction (PCR), Western blot, and immunohistochemical analysis. The methylation of PRDM promoters was detected by methylation-specific PCR. The correlation of methylation and expression of PRDMs with clinicopathological characteristics of patients were analyzed.
Results: mRNA expression of PRDM2, PRDM5, and PRDM16 was low or absent in tumor tissues compared to distant lung tissues. The methylation frequencies of PRDM2, PRDM5, and PRDM16 in tumor tissues were significantly higher than those in distal lung tissues. In LSCC patients, methylation of PRDM2 and PRDM16 was correlated with smoking status and methylation of PRDM5 was correlated with tumor differentiation.
Conclusion: The expression of PRDM2, PRDM5, and PRDM16 is low or absent in NSCLC, and this is mainly due to gene promoter methylation. Smoking may be an important cause of PRDM2 and PRDM16 methylation in NSCLC.

Keywords: lung tumor, PR domain zinc finger protein, epigenetics, methylation, gene expression

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