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Expression and clinicopathological significance of EED, SUZ12 and EZH2 mRNA in colorectal cancer

  • Original Article - Cancer Research
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Abstract

Background and objectives

Enhancer of zeste 2 (EZH2), embryonic ectoderm development (EED), and suppressor of zeste 12 homolog (SUZ12), the key component of polycomb repressive complex 2, are of great importance in human cancer pathogenesis. This study was designed to investigate the clinical and prognostic significances of EZH2, EED and SUZ12 in colorectal cancer (CRC) patients.

Methods

The expression of EZH2, EED and SUZ12 mRNA was evaluated in 82 primary CRC and paired non-cancerous mucosa samples by qRT-PCR.

Results

We found that overall EZH2, EED and SUZ12 mRNA expression in the CRC tissues was significantly increased than in the non-cancerous tissue (p < 0.05). Increased EZH2, EED and SUZ12 mRNA expression was directly correlated with primary tumor size, regional lymph node metastases, distant metastasis and AJCC stage. Furthermore, CRC patients with higher level of EED, SUZ12 or EZH2 showed a worse disease-free survival (DFS) (p < 0.01). In multivariate analysis, the increased EZH2 expression may be a risk factor for the patients’ 3-year DFS (HR 2.517; 95 % CI 1.104, 5.736; p = 0.028). Furthermore, the k-means cluster analysis showed that high mRNA expression of EED, SUZ12 and EZH2 was significantly correlated with the aggressive clinical behavior and poor prognosis.

Conclusions

High expression of EED, SUZ12 and EZH2 might contribute to the CRC development/progression.

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Acknowledgments

This study was supported by NSFC (81372939), NSFC (81272704), Heilongjiang postdoctoral fund (LBH-Z12155) and by SRFDP (20132307120012).

Conflict of interest

None.

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Authors

Corresponding authors

Correspondence to Bin-Bin Cui or Yan-Mei Yang.

Additional information

Yan-Long Liu, Xu Gao and Yang Jiang have contributed equally to the work.

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Liu, YL., Gao, X., Jiang, Y. et al. Expression and clinicopathological significance of EED, SUZ12 and EZH2 mRNA in colorectal cancer. J Cancer Res Clin Oncol 141, 661–669 (2015). https://doi.org/10.1007/s00432-014-1854-5

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  • DOI: https://doi.org/10.1007/s00432-014-1854-5

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