Differential expression of phospholipase C epsilon 1 is associated with chronic atrophic gastritis and gastric cancer

PLoS One. 2012;7(10):e47563. doi: 10.1371/journal.pone.0047563. Epub 2012 Oct 15.

Abstract

Background: Chronic inflammation plays a causal role in gastric tumor initiation. The identification of predictive biomarkers from gastric inflammation to tumorigenesis will help us to distinguish gastric cancer from atrophic gastritis and establish the diagnosis of early-stage gastric cancer. Phospholipase C epsilon 1 (PLCε1) is reported to play a vital role in inflammation and tumorigenesis. This study was aimed to investigate the clinical significance of PLCε1 in the initiation and progression of gastric cancer.

Methodology/principal findings: Firstly, the mRNA and protein expression of PLCε1 were analyzed by reverse transcription-PCR and Western blotting in normal gastric mucous epithelial cell line GES-1 and gastric cancer cell lines AGS, SGC7901, and MGC803. The results showed both mRNA and protein levels of PLCε1 were up-regulated in gastric cancer cells compared with normal gastric mucous epithelial cells. Secondly, this result was confirmed by immunohistochemical detection in a tissue microarray including 74 paired gastric cancer and adjacent normal tissues. Thirdly, an independence immunohistochemical analysis of 799 chronic atrophic gastritis tissue specimens demonstrated that PLCε1 expression in atrophic gastritis tissues were down-regulated since PLCε1 expression was negative in 524 (65.6%) atrophic gastritis. In addition, matched clinical tissues from atrophic severe gastritis and gastric cancer patients were used to further confirm the previous results by analyzing mRNA and protein levels expression of PLCε1 in clinical samples.

Conclusions/significances: Our results suggested that PLCε1 protein may be a potential biomarker to distinguish gastric cancer from inflammation lesion, and could have great potential in applications such as diagnosis and pre-warning of early-stage gastric cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Diagnosis, Differential
  • Early Detection of Cancer*
  • Gastritis, Atrophic* / diagnosis
  • Gastritis, Atrophic* / genetics
  • Gene Expression
  • Humans
  • Inflammation
  • Phosphoinositide Phospholipase C / genetics*
  • Phosphoinositide Phospholipase C / metabolism
  • Stomach Neoplasms* / diagnosis
  • Stomach Neoplasms* / genetics

Substances

  • Biomarkers, Tumor
  • Phosphoinositide Phospholipase C
  • phospholipase C epsilon

Grants and funding

This work was supported by National Key Basic Research Program of China (973 Project) (2010CB933900), New Century Excellent Talent of Ministry of Education of China (NCET-08-0350), Special Infection Diseases Key Project of China (2009ZX10004-311), National Natural Science Foundation of China (31170961 and 31100717), Shanghai Science and Technology Fund (12ZR1415800) and Shanghai Jiao Tong University Innovation Fund For Postgraduates (Z-340-007). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.