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2 results on '"Kang, Huijie"'

1. Author Correction: Enah overexpression is correlated with poor survival and aggressive phenotype in gastric cancer.

Author

Chen D, Xu L, Li X, Chu Y, Jiang M, Xu B, Zhao M, Wang W, Wang H, Kang H, Wang K, Wu K, Liang J, and Ren G

Abstract

In the version of this article originally submitted, Fig 5j included a mismatched image which had been accidentally inserted by the authors during collation of the data. The final data was derived from three independent experiments, and three repetitions for each experiment to ensure the repeatability, reliability and scientificity of the experiment. During this process, the fields overlapped to some extent, giving rise to the mistake. It does not alter any inferences drawn from the data, and the statistical graph is correct. This error has been corrected in both the PDF and HTML versions of the Article.

Published
2019
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2. Enah overexpression is correlated with poor survival and aggressive phenotype in gastric cancer.

Author

Chen D, Xu L, Li X, Chu Y, Jiang M, Xu B, Zhao M, Wang W, Wang H, Kang H, Wang K, Wu K, Liang J, and Ren G

Subjects
Animals, Apoptosis, Cell Line, Tumor, Cell Movement, Cell Proliferation, Epithelial-Mesenchymal Transition, Female, Gene Knockdown Techniques, Heterografts, Humans, Kaplan-Meier Estimate, MAP Kinase Signaling System, Male, Mice, Microfilament Proteins genetics, Middle Aged, NF-kappa B metabolism, Neoplasm Metastasis physiopathology, Neoplasm Staging, Proto-Oncogene Proteins c-akt metabolism, Stomach Neoplasms mortality, Stomach Neoplasms pathology, Transfection, Microfilament Proteins metabolism, Stomach Neoplasms metabolism
Abstract

Enabled homolog (Enah), which is a member of the Ena/VASP family that also includes VASP (vasodilator-stimulated phosphoprotein) and Ena/VASP like, is a mammalian ortholog of Drosophila Enabled (Ena). An increasing number of studies demonstrated Enah overexpression is involved in human colorectal carcinomas, breast cancers and hepatocellular carcinoma. However, the significance of Enah expression in gastric cancer (GC) is poorly elucidated. Here, we demonstrate that Enah is upregulated in GC and associated with AJCC stage, depth of invasion and poor overall survival (OS). Knockdown of Enah inhibited GC cell proliferation and metastasis and vice versa. Further experiments suggested that p-Erk1/2, p-AKT, p-p65, Vimentin and Fibronectin were downregulated and E-cadherin was upregulated after Enah silencing, implicating altered functions in GC proliferation and metastasis. Thus, our study suggests that Enah is a harmful factor for GC and a novel target for GC treatment.

Published
2018
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