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SOX2 in Gastric Carcinoma, but not Hath1, is Related to Patients’ Clinicopathological Features and Prognosis

  • Original Article
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Journal of Gastrointestinal Surgery

Abstract

Background

SOX2 and Hath1 are transcription factors that are critical for the control of terminal cell differentiation in the gastrointestinal mucosa. This study investigated the correlations between SOX2 and Hath1 expression in gastric carcinoma and patients’ clinicopathological features and prognosis.

Methods

Hath1 and SOX2 were detected by immunohistochemistry in gastric carcinoma (n = 50). Probability of survival of patients after surgery was estimated by the Kaplan–Meier method and compared using Log-rank test.

Results

Hath1 and SOX2 were inversely expressed in gastric carcinoma. Patients with strong SOX2 expression (++ to +++) showed lower incidences of lymph node metastasis (p = 0.007), deeper invasion (p = 0.010), and III–IV clinical stages (p = 0.011) compared to patients with low SOX2 expression (− to +). There was no significant difference in SOX2 and Hath1 expression in the cancerous tissues of the patients with and without Helicobacter pylori infection (p > 0.05). The patients with strong expression of SOX2 in their cancerous tissues (++ to +++) had a better prognosis than those with low expression of SOX2 (− to +; p = 0.005). There was no correlation between Hath1 expression level and prognosis (p = 0.676).

Conclusions

SOX2 and Hath1 are inversely expressed in gastric carcinoma. SOX2 provides a survival advantage to patients of gastric carcinoma and appears to be associated with metastasis and clinical stages.

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Correspondence to Rongquan Wang.

Additional information

The study was supported by the Natural Science Foundation Project of CQ CSTC 2008BA5034.

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Zhang, X., Yu, H., Yang, Y. et al. SOX2 in Gastric Carcinoma, but not Hath1, is Related to Patients’ Clinicopathological Features and Prognosis. J Gastrointest Surg 14, 1220–1226 (2010). https://doi.org/10.1007/s11605-010-1246-3

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  • DOI: https://doi.org/10.1007/s11605-010-1246-3

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