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Updated: Jun 20, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Upregulation of human DNA binding protein A (dbpA) in gastric cancer cells
Guo-rong Wang1, Yan Zheng, Xiang-ming Che
1Department of General Surgery, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an 710061, China.
Aim:
To determine the effect of human DNA binding protein (dbpA) on the biology of gastric cancer cells.
Methods:
DbpA expression was analyzed by Western blot analysis and immunofluorescence staining in gastric cancer tissues and cell lines. A dbpA-specific small interference (si) RNA was designed and synthesized. Suppressive effect of siRNA on dbpA expression was assessed by real-time RT-PCR. Transwell migration and colony formation assays were used to assess the inhibitory effects of dbpA siRNA on cell invasion and tumorigenesis in vitro. Drug-sensitivity was evaluated using a conventional 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay.
Results:
The expression of dbpA was upregulated in gastric cancer tissues and cell lines as compared to adjacent normal tissues or gastric epithelial cells. siRNA treatment successfully silenced dbpA expression. Silencing of dbpA increased expression of E-cadherin, decreased expression of adenomatous polyposis coli (APC), beta-catenin and cyclin D1, but had no effect on expression of NF-kappaB. Silencing of dbpA also suppressed cell invasion and colony formation of SGC7901 cells, and enhanced their chemosensitivity to 5-fluorouracil.
Conclusion:
DbpA plays an important role in the pathogenesis and development of gastric cancer, and the process involves E-cadherin, APC, beta-catenin and cyclin D1. Silencing of dbpA might be a novel therapeutic strategy for increasing chemosensitivity to 5-fluorouracil in gastric cancer.
Insights
Human DNA binding protein (dbpA) is upregulated in gastric cancer, promoting cell invasion and tumorigenesis. Silencing dbpA inhibits cancer cell growth and enhances sensitivity to 5-fluorouracil, suggesting a new therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Gastric cancer is a significant global health concern.
- The role of specific proteins in gastric cancer pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the effect of human DNA binding protein (dbpA) on gastric cancer cell biology.
- To explore the potential of targeting dbpA for gastric cancer therapy.
Main Methods:
- Analyzed dbpA expression in gastric cancer tissues and cell lines using Western blot and immunofluorescence.
- Utilized small interfering RNA (siRNA) to silence dbpA expression and assessed its effects on cell invasion, colony formation, and drug sensitivity (5-fluorouracil) via Transwell, colony formation, and MTT assays.
- Examined the impact of dbpA silencing on key molecular markers including E-cadherin, APC, beta-catenin, cyclin D1, and NF-kappaB using real-time RT-PCR.
Main Results:
- DbpA expression was significantly upregulated in gastric cancer tissues and cell lines compared to normal controls.
- siRNA-mediated silencing of dbpA suppressed gastric cancer cell invasion and colony formation in vitro.
- Silencing dbpA modulated the expression of E-cadherin, APC, beta-catenin, and cyclin D1, and notably enhanced chemosensitivity to 5-fluorouracil.
Conclusions:
- DbpA plays a crucial role in gastric cancer pathogenesis and development, influencing key cellular pathways.
- Targeting dbpA through silencing presents a promising therapeutic strategy to enhance chemosensitivity in gastric cancer treatment.
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