Differential regulation of LRRC37A2 in gastric cancer by DNA methylation

Epigenetics. 2022 Jan;17(1):110-116. doi: 10.1080/15592294.2021.1878724. Epub 2021 Feb 8.

Abstract

Gastric cancer (GC) is one of the leading types of fatal cancer worldwide. Epigenetic manipulation of cancer cells is a useful tool to better understand gene expression regulatory mechanisms and contributes to the discovery of novel biomarkers. Our research group recently reported a list of 83 genes that are potentially modulated by DNA methylation in GC cell lines. Herein, we further explored the regulation of one of these genes, LRRC37A2, in clinical samples. LRRC37A2 expression was evaluated by RT-qPCR, and DNA methylation was studied using next-generation bisulphite sequencing in 36 GC and paired adjacent nonneoplastic tissue samples. We showed that both reduced LRRC37A2 mRNA levels and increased LRRC37A2 exon methylation were associated with undifferentiated and poorly differentiated tumours. Moreover, LRRC37A2 gene expression and methylation levels were inversely correlated at the +45 exon CpG site. We suggest that DNA hypermethylation may contribute to reducing LRRC37A2 expression in undifferentiated and poorly differentiated GC. Therefore, our results show how some genes may be useful to stratify patients who are more likely to benefit from epigenetic therapy.Abbreviations: AR: androgen receptor; 5-AZAdC: 5-aza-2'-deoxycytidine; B2M: beta-2-microglobulin; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GC: gastric cancer; GLM: general linear model; LRRC37A2: leucine-rich repeat containing 37 member A2; SD: standard deviation; TFII-I: general transcription factor II-I; TSS: transcription start site; XBP1: X-box binding protein 1.

Keywords: DNA methylation; LRRC37A2; cancer therapy; gene expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • CpG Islands
  • DNA Methylation*
  • Decitabine
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Stomach Neoplasms* / genetics
  • Stomach Neoplasms* / metabolism

Substances

  • Decitabine

Grants and funding

This study was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo [FAPESP, Processo n° 2016/19953-6 to FW, Processo n° 2017/06227-8 to JCG, Processo n° 2007/02470-3 to MFL, Processo n° 2010/11174-1 to DQC, and Processo n° 2009/07145-9 to MACS], the Conselho Nacional de Desenvolvimento Científico e Tecnológico [CNPq; to FW, DQC, JCG, RRB, and MACS], and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior [CAPES; to COG and ACA].