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.
Highlights
Gastric cancer (GC) is the fourth most common cancer and the second most common cause of cancer-related death[1]
To determine the role of Enabled homolog (Enah) in GC, firstly, the Oncomine database was queried and the results showed that Enah mRNA expression was higher in GC tissues compared with corresponding normal tissues (Fig. 1a) and Enah copy number was increased in GC tissues (Fig. 1b).we obtained thirty-nine paired GC tissues and corresponding normal tissues for qRT-PCR and as shown in Fig. 1c, in comparison with normal tissues, the expression level of Enah mRNA is significantly higher in GC tissues
We found that Enah positive rate was 84.44% (76/ 90) in GC tissues and 51.11% (46/90) in non-cancerous adjacent tissues with a significantly statistical difference (p < 0.001, Table 1) and Enah was mainly present in the cytoplasm of tumor cells (Fig. 1d)
Summary
Gastric cancer (GC) is the fourth most common cancer and the second most common cause of cancer-related death[1]. Approximately 990,000 people are diagnosed with GC in the world, of whom about 738,000 die from this disease[2,3]. GC incidence rates differ in sexes and nations. Rates are two to three folds higher in men than women[2], and the highest incidence rates are observed in East Asia, East Europe, and South America, while the lowest rates in North America and most parts of Africa[4]. With the combination of chemotherapy, radiotherapy and surgery treatment, the quality of life of GC patients has improved, but the prognosis of GC patients still makes people feel dissatisfactory. It is very important for us to look for better biomarkers to diagnose, guide clinical treatment and predict prognosis for GC.
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