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Overexpression of SMYD3 was associated with increased STAT3 activation in gastric cancer

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Abstract

This study aimed to investigate mRNA and protein expressions of SET and MYND domain-containing protein 3 (SMYD3), STAT3, and phosphorylated STAT3 (pSTAT3) in gastric cancer (GC). This study was also conducted to explore the correlations between these proteins and biological behaviors of GC. SMYD3, STAT3, and pSTAT3 expressions were detected in GC tissues and adjacent non-tumor tissues by semiquantitative/quantitative reverse transcription polymerase chain reaction and Western blot analysis. SMYD3, STAT3, and pSTAT3 expressions in tissue sections were evaluated by immunohistochemistry. Staining results were compared with clinicopathological characteristics and the outcome of patients. The mRNA expression levels of SMYD3 or STAT3 and the protein expression levels of SMYD3, STAT3, or pSTAT3 in GC tissues were significantly higher than those in adjacent non-tumor tissues. Lymph node metastasis was identified as an independently relative factor for SMYD3 expression; the degree of differentiation and serosal invasion were identified as the independently relative factors for pSTAT3 expression in GC tissues. SMYD3 expression and STAT3 or pSTAT3 expressions in GC tissues were significantly and positively correlated. Multivariate analysis results demonstrated that primary tumor location, lymph node metastasis, SMYD3 expression, and pSTAT3 expression were independent prognostic indicators of GC. pSTAT3 expression was an optimal prognostic predictor of patients, as identified by Cox regression with Akaike’s information criterion value calculation. High SMYD3 and pSTAT3 expressions may indicate poor prognosis of patients with GC.

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Acknowledgments

This work was supported by National Natural Science Foundation of China (No. 31470816).

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Correspondence to Han Liang.

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Deng Jingyu is the Joint First Author.

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Liu, Y., Deng, J., Luo, X. et al. Overexpression of SMYD3 was associated with increased STAT3 activation in gastric cancer. Med Oncol 32, 404 (2015). https://doi.org/10.1007/s12032-014-0404-y

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