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Oncol Lett. 2017 Mar;13(3):1360-1364. doi: 10.3892/ol.2017.5558. Epub 2017 Jan 02.

Aberrant KLK4 gene promoter hypomethylation in pediatric hepatoblastomas.

Oncology letters

Baihui Liu, Ximao Cui, Shan Zheng, Kuiran Dong, Rui Dong

Affiliations

  1. Department of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defects and Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai 201102, P.R. China.

PMID: 28454262 PMCID: PMC5403249 DOI: 10.3892/ol.2017.5558

Abstract

DNA methylation has a crucial role in cancer biology and has been recognized as an activator of oncogenes and inactivator of tumor suppressor genes, both of which are mechanisms for tumorigenesis. Kallikrein-related peptidase 4 (KLK4), has been suggested to be an oncogene in various types of cancer. The aim of the present study was to assess the DNA methylation patterns of the KLK4 gene in cancerous samples harvested from patients with hepatoblastoma (HB). KLK4 mRNA expression levels were detected using reverse transcription-quantitative polymerase chain reaction and assessed its DNA methylation patterns using high-throughput mass spectrometry on a matrix-assisted laser desorption/ionization time-of-flight mass array. A total of 10 HB and 10 normal liver tissue samples were obtained from patients with HB. The results of the present study showed that a significantly higher level of KLK4 mRNA expression levels were detected in HB tissues, as compared with the matched controls. Furthermore, the KLK4 gene promoter region was distinctively less methylated in the HB samples compared with the controls and negatively correlated with KLK4 mRNA expression levels. These findings indicate that aberrant methylation of KLK4 may contribute to its upregulated mRNA expression in HB.

Keywords: DNA methylation; hepatoblastoma; kallikrein-related peptidase 4; matrix-assisted laser desorption/ionization time-of-flight

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