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Expression of NGF family and their receptors in gastric carcinoma: a cDNA microarray study
Jian-Jun Du1, Ke-Feng Dou, Shu-You Peng
1Department of General Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shanxi Province, China.
Aim:
To investigate the expression of NGF family and their receptors in gastric carcinoma and normal gastric mucosa, and to elucidate their effects on gastric carcinoma.
Methods:
RNA of gastric cancer tissues and normal gastric tissues was respectively isolated and mRNA was purified. Probes of both mRNA reverse transcription product cDNAs labeled with alpha-(33)P dATP were respectively hybridized with Atlas Array membrane where NGF and their family genes were spotted on. Hybridized signal images were scanned on phosphor screen with ImageQuant 5.1 software after hybridization. Normalized values on spots were analyzed with ArrayVersion 5.0 software. Differential expression of NGF family and their receptors mRNA was confirmed between hybridized Atlas Array membranes of gastric cancer tissues and normal gastric mucosa, then their effects on gastric carcinoma were investigated.
Results:
Hybridization signal images on Atlas Array membrane appeared in a lower level of nonspecific hybridization. Both of NGF family and their receptors Trk family mRNA were expressed in gastric cancer and normal gastric mucosa. But adversely up-regulated expression in other tissues and organs. NGF, BDGF, NT-3, NT-4/5, NT-6 and TrkA, B and C were down-regulated simultaneously in gastric carcinoma in comparison with normal gastric mucosa. Degrees of down-regulation in NGF family were greater than those in their receptors Trk family. Down-regulation of NT-3 and BDGF was the most significant, and TrkC down-regulation level was the lowest in receptors Trk family.
Conclusion:
Down-regulated expression of NGF family and their receptors Trk family mRNA in gastric cancer is confirmed. NGF family and their receptors Trk family probably play a unique role in gastric cancer cell apoptosis by a novel Ras or Raf signal transduction pathway. Their synchronous effects are closely associated with occurrence and development of gastric carcinoma induced by reduction of signal transduction of programmed cell death.
Insights
Nerve Growth Factor (NGF) family and their receptors are downregulated in gastric cancer. This suggests a role in cancer cell apoptosis and development through altered signaling pathways.
Area of Science:
- Molecular Biology
- Oncology
- Gene Expression Analysis
Background:
- The Nerve Growth Factor (NGF) family and their receptors play crucial roles in neuronal development and function.
- Altered expression of these factors has been implicated in various cancers, but their specific role in gastric carcinoma remains to be fully elucidated.
Purpose of the Study:
- To investigate the expression patterns of the NGF family and their receptors in gastric carcinoma compared to normal gastric mucosa.
- To determine the functional implications of these factors in the development and progression of gastric cancer.
Main Methods:
- RNA extraction from gastric cancer and normal tissues.
- mRNA purification and cDNA synthesis.
- Atlas Array membrane hybridization with labeled probes for NGF family and receptor genes.
- Image scanning and data analysis using specialized software to assess gene expression levels.
Main Results:
- Both NGF family members and Trk receptors were expressed in both gastric cancer and normal tissues.
- A significant downregulation of NGF, BDNF, NT-3, NT-4/5, NT-6, TrkA, TrkB, and TrkC mRNA was observed in gastric carcinoma compared to normal gastric mucosa.
- The downregulation of NGF family members was more pronounced than that of their Trk receptors, with NT-3 and BDNF showing the most significant decrease.
Conclusions:
- The study confirms the downregulated expression of NGF family and Trk receptor mRNAs in gastric cancer.
- These factors likely influence gastric cancer cell apoptosis via novel Ras or Raf signal transduction pathways.
- The synchronous downregulation is closely associated with gastric carcinoma occurrence and development, potentially by reducing programmed cell death signaling.