Research Papers:

ERK expression and its correlation with STAT1 in esophageal squamous cell carcinoma

Hu Wang, Ying Zhang, Hailong Yun, Shubiao Chen, Yelong Chen and Zhaoyong Liu _

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Oncotarget. 2017; 8:45249-45258. https://doi.org/10.18632/oncotarget.16902

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Hu Wang1,*, Ying Zhang2,*, Hailong Yun2, Shubiao Chen1, Yelong Chen1 and Zhaoyong Liu1

1Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

2Department of Pathology, Shantou University Medical College, Shantou, Guangdong Province, China

*These authors contributed equally to this work

Correspondence to:

Zhaoyong Liu, email: [email protected]

Keywords: ESCC, ERK, p-ERK STAT1, immunohistochemistry

Received: September 20, 2016     Accepted: March 27, 2017     Published: April 06, 2017


Background: Esophageal squamous cell carcinoma is one of leading causes of cancer-related deaths in Chaoshan region a high-risk region for esophageal cancer. Extracellular regulated protein kinases (ERK) usually play an important role in cell proliferation and differentiation. However, accumulating evidence has shown that the ERK was aberrantly expressed in cancers and correlated with STAT1 depression.

Results: The activated ERK downregulates STAT1 expression in ESCC cell lines and U0126 increases expression of STAT1. Our immunohistochemistry result also confirms that the expression of ERK inversely correlated with that of STAT1 in ESCC tumors. In addition, a significantly higher expression of ERK/p-ERK was found in ESCC tissues in comparison with case-matched normal esophageal tissues (p < 0.05). Moreover, the immunohistochemical analysis demonstrated that ERK expression was paralleled with the differentiation and clinical stage. In 74 patients with follow-up data, those with ERKlow tumors survived significantly longer than those with ERKhigh tumors (p = 0.04); patients with ERKlow/STAT1high tumors had the longest survival (p = 0.001).

Materials and Methods: To investigate whether ERK can mediated STAT1 expression in ESCC, we used the MEK plasmid and U0126, a MEK inhibitor, to treat the cell. To further confirm our in-vitro study, we detected the ERK, p-ERK and STAT1 expression in 131 ESCC cases and 22 case-matched normal esophageal tissues adjacent to the tumors specimens.

Conclusions: These findings provide pathological evidence that ERK/p-ERK is negatively correlated with STAT1 in ESCC. Our data suggests that inhibition of ERK and/or restoration of STAT1 expression maybe useful therapeutic strategies for ESCC.

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