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Loss of opioid binding protein/cell adhesion molecule-like gene expression in gastric cancer
Ning Zhang1, Jide Xu2, Yuhong Wang3
1Department of Respiratory Disease, Affiliated LuoHu Hospital of Shenzhen University, Shenzhen, Guangdong 518001, P.R. China.
Abstract:
Previous studies have reported that the expression of the opioid binding protein/cell adhesion molecule-like (OPCML) gene was frequently downregulated in various of types of cancer. However, little is known regarding the expression of the OPCML gene in gastric cancer. The present study identified that OPCML was downregulated in the gastric cancer SGC7901, KATO III, MKN45, MKN74, SNU1, AGS, N87 and a gastric mucosa cell line GES1, compared with normal gastric tissues by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). To investigate whether the downregulation of OPCML was due to promoter hypermethylation, the methylation of the OPCML promoter was assessed by methylation-specific polymerase chain reaction. Hypermethylation of the OPCML promoter was observed in the gastric cancer MKN45 cell lines, but was not as evident in normal gastric tissue. The methylation inhibitor 5-aza-2'-deoxycytidine was used to remove the methylation of the OPCML gene promoter, following which the expression of OPCML was restored. In addition, the function of the OPCML gene was studied in vitro, and it was found that the restoration expression of OPCML could lead to the suppression of cell growth. In conclusion, the present study has shown that OPCML, which acts as a tumor suppressor, was silenced in gastric cancer cell lines via aberrant hypermethylation of the promoter CpG islands, which may provide a novel molecular approach for the early diagnosis of gastric cancer.
Insights
The opioid binding protein/cell adhesion molecule-like (OPCML) gene is downregulated in gastric cancer due to promoter hypermethylation. Restoring OPCML expression suppresses tumor growth, suggesting its role as a tumor suppressor for early gastric cancer diagnosis.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Opioid binding protein/cell adhesion molecule-like (OPCML) gene expression is often reduced in various cancers.
- The role and expression patterns of OPCML in gastric cancer remain largely uncharacterized.
Purpose of the Study:
- To investigate OPCML gene expression in gastric cancer.
- To determine if promoter hypermethylation contributes to OPCML downregulation.
- To explore the functional role of OPCML in gastric cancer cell growth.
Main Methods:
- Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to assess OPCML expression.
- Methylation-specific polymerase chain reaction to analyze OPCML promoter methylation.
- Treatment with 5-aza-2'-deoxycytidine to evaluate the effect of promoter demethylation.
- In vitro studies to assess the impact of OPCML restoration on cell growth.
Main Results:
- OPCML expression was significantly downregulated in multiple gastric cancer cell lines compared to normal gastric tissues.
- Hypermethylation of the OPCML promoter was observed in gastric cancer cells, correlating with reduced expression.
- Demethylation using 5-aza-2'-deoxycytidine restored OPCML expression.
- Restoration of OPCML expression led to the suppression of gastric cancer cell growth.
Conclusions:
- OPCML functions as a tumor suppressor in gastric cancer.
- Aberrant hypermethylation of OPCML promoter CpG islands silences its expression in gastric cancer.
- OPCML may serve as a potential biomarker for early gastric cancer diagnosis.
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