Abstract
BackgroundMetastasis is the main cause of death in patients with advanced stage colon cancer. Epithelial mesenchymal transition (EMT) plays an important role in invasion and metastasis. Actin-like 6A (ACTL6A) is vital for embryogenesis and differentiation and is also critical for metastasis and EMT in hepatocellular carcinoma, as observed in our previous study. In the present study, we further explored the role of ACTL6A in colon cancer metastasis.MethodsACTL6A expression levels were analyzed in normal colon, colon adenoma and colon cancer specimens using public databases and tissue samples. ACTL6A expression and its association with clinicopathologic features of colon cancer patients were also analyzed. ACTL6A-overexpression and ACTL6A-knockdown colon cancer cells were used to perform cytological experiments to explore the potential biological function of ACTL6A in metastasis and EMT in colon cancer.ResultsThe data from both the Gene Expression Omnibus (GEO) and Oncomine databases showed that ACTL6A expression levels in colon adenoma and cancer were higher than those in normal colon samples. The ACTL6A expression level in fresh colon cancer specimens was also higher than that in the corresponding adjacent normal colon specimens. Patients with high ACTL6A expression directly correlated with advanced pT status, distant metastasis, poor differentiation and microvascular/perineural invasion. ACTL6A overexpression promoted migration and invasion of colon cancer cells, whereas ACTL6A knockdown exhibited the opposite effect in vitro. Moreover, we demonstrated that ACTL6A promoted EMT in colon cancer cells in vitro.ConclusionsOur findings indicate that ACTL6A exhibits pro-tumor function and acts as an EMT activator in colon cancer. ACTL6A may serve as a potential therapeutic target for colon cancer.
Highlights
Metastasis is the main cause of death in patients with advanced stage colon cancer
Actin-like 6A (ACTL6A) expression was upregulated in colon cancer from public databases We first explored ACTL6A expression in colon adenoma and colon cancer using the Gene Expression Omnibus (GEO) database by searching “ACTL6A and colon cancer”
Seventeen pairs of cancer and noncancerous tissues from surgically resected colon cancer were analyzed in another GEO database GDS 4382; the results showed that the ACTL6A signal intensity in the cancer tissue was significantly higher than that in the paired noncancerous tissue (Fig. 1b, p < 0.001)
Summary
Epithelial mesenchymal transition (EMT) plays an important role in invasion and metastasis. We further explored the role of ACTL6A in colon cancer metastasis. In the last 2 decades, within imaging techniques and therapeutic strategies advance, the 5-year survival rate for all stages of colon cancer has increased to 66%. The survival rate for distant-stage colon cancer is still very poor, the 2-year survival rate is only approximately 20–30% mainly due to metastasis [1, 2]. Metastasis is a multistep invasion metastasis cascade, composed of local invasion, intravasation, survival in the circulation, arrest at a distant organ site, extravasation, initial survival in a foreign microenvironment and micrometastasis formation, and metastatic colonization. Increasing evidence has suggested that epithelial mesenchymal transition (EMT) plays an important role in this pathological process, especially in the initiation of local invasion [3]. EMT enhances cell motility, migration, invasiveness and resistance to apoptosis, which endows cancer
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