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Hypermethylation and aberrant expression of transcription factor SOX7 gene in gastric cardia adenocarcinoma
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Abstract:
Objective:To determine the methylation status and expression of SOX7 gene in association with Wnt signaling and clinicopathological characteristics in gastric cardia adenocarcinoma (GCA). Methods: Paired specimens of primary tumor and corresponding adjacent tissues were collected from 130 patients who were diagnosed with GCA and underwent surgical ablation in the Thoracic Surgery, Fourth Hospital Affiliated to Hebei Medical University in Shijiazhuang between 2006 and 2012. Methylation of CpG sites within the SOX7 gene promoter was assessed by methylation specific PCR (MSP), SOX7 mRNA abundance by RT-PCR, and β-catenin protein by immunohistochemistry, in these speciments. Associations of the methylation status of the SOX7 gene promoter with SOX7 mRNA abundance, β-catenin protein contents, clinicopathologic variables and the history of the upper gastrointestinal cancers (UGIC), respectively, were assessed. Results: The frequency of SOX7 gene methylation was significantly higher in GCA tissue (57.7%) than that in the adjacent non-cancerous tissues ( P <0.01). The hypermethylation of this gene was correlated with lymph node metastasis ( P <0.05) but neither with pathological grade nor clinical stage ( P >0.05). SOX7 mRNA abundance was significantly lower in GCA tissue (0.414±0.054) than that in the corresponding adjacent tissues (0.695±0.034, P <0.01). The ectopic expression frequency of β-catenin was significantly different between GCA and adjacent tissue specimens (85.4% vs 43.1%, P <0.05). SOX7 mRNA and β-catenin protein levels were significantly correlated with the frequency of SOX7 gene methylation in GCA tissue ( P <0.05). In addition，the methylation status of the SOX7 gene was closely related with the history of UGIC ( P <0.01). Conclusion: Hypermethylation of CpG sites within the SOX7 gene promoter and the resultant aberration of canonical Wnt/β-catenin signaling may play an important role in the pathogenesis of GCA.
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Project Supported:
Project supported by the Natural Science Foundation of Hebei Province (No.H2013206315), and the Focal Point Project of Hebei Medical Research（No.20130543）
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