Abstract
To investigate the expression of miR-23a and metastasis suppressor 1 (MTSS1) and their clinical significance in colon carcinoma. A total of 92 cases of colon carcinomas were collected with both the tumor and paired normal tissue samples for the study. The miR-23a targeting MTSS1 was evaluated by luciferase reporter vector. Cell invasion potential was evaluated by trans-well invasion assay. In-situ hybridization and immunohistochemistry were used to detect miR-23a and MTSS1 expression. MiR-23a downregulated the expression of MTSS protein and enhanced the invasiveness of colon carcinoma. The expression rates of miR-23a and MTSS1 were 87.0% (80/92) and 17.4% (16/92) in colon carcinoma cases, respectively (P < 0.01). The up-regulation of miR-23a expression was associated with an advanced clinical stage (P = 0.029) and depth of invasion (P = 0.000). The expression of miR-23a was higher in the tumors with lymph node metastasis than those without (P = 0.041). Down-regulation of MTSS1 expression was associated with an advanced clinical stage (P = 0.027) and depth of invasion (P = 0.017). The expression of MTSS1 was lower in the tumors with lymph node metastasis than those without (P = 0.009). The expression of miR-23a had significantly negative correlation with that of MTSS1 (r = -0.594, P = 0.013). MiR-23a expression promotes colon carcinoma cell growth, invasion and metastasis through inhibition of MTSS gene. Both the low expression of MTSS1 and high expression of miR-23a may serve as important biological markers for the malignant phenotypes of colon cancer, such as invasion and metastasis.
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