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HTRA1 gene expression in gastric epithelial cells
Hong-Xue Wu1, Shi-Lun Tong1, Chong Wu1
1Gastrointestinal Department, People's Hospital Affiliated to Wuhan University, Wuhan 430060, Hubei Province, P.R. China.
Asian Pacific Journal of Tropical Medicine
|August 18, 2014
Summary
HtrA1 gene expression is down-regulated in gastric cancers due to epigenetic silencing. Reactivating HtrA1 may offer a new strategy for gastric cancer chemotherapy.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- HtrA1 is a serine protease involved in tumor suppression.
- Altered HtrA1 expression is observed in various cancers.
Purpose of the Study:
- To investigate HtrA1 gene expression and its regulatory mechanisms in human gastric cancers.
- To explore the potential of HtrA1 re-activation in gastric cancer therapy.
Main Methods:
- Quantitative PCR (QPCR) and Northern blot for HtrA1 mRNA analysis.
- Western blot for HtrA1 protein detection.
- Bisulfite sequencing to assess promoter DNA methylation status.
- RT-PCR to evaluate the effect of decitabine and TSA on HtrA1 expression.
Main Results:
- HtrA1 expression was significantly down-regulated in gastric carcinoma tissues and cell lines compared to normal epithelium.
- HtrA1 promoter region showed hypermethylation in gastric cancer cells.
- HtrA1 protein was undetectable in gastric cancer cell lines but present in normal gastric epithelial cells.
- Decitabine and TSA treatment partially restored HtrA1 expression in gastric cancer cells.
Conclusions:
- Epigenetic silencing, specifically DNA methylation, contributes to HtrA1 down-regulation in gastric cancer.
- Re-activating HtrA1 gene expression via epigenetic modification presents a potential therapeutic strategy for gastric cancer.
- Further research into HtrA1's role in chemotherapy is warranted.
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