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Abstract
While it is known that miR-203 is frequently downregulated in many types of human cancer, little is known regarding its expression and functional role in colorectal cancer (CRC). In this study, we aimed to investigate the expression and the potential mechanisms of miR-203 in colorectal cancer. MiR-203 was significantly downregulated in CRC tissues compared with matched normal adjacent tissues. Our clinical data show that decreased miR-203 was associated with an advanced clinical tumor-node-metastasis stage, lymph node metastasis, and poor survival in CRC patients. Furthermore, externally induced expression of miR-203 significantly inhibited CRC cell proliferation and invasion in vitro and in vivo. Mechanistically, we identified EIF5A2 as a direct and functional target of miR-203. The levels of miR-203 were inversely correlated with levels of the EIF5A2 in the CRC tissues. Restoration of EIF5A2 in the miR-203-overexpressing CRC cells reversed the suppressive effects of miR-203. Our results demonstrate that miR-203 serves as a tumor suppressor gene and may be useful as a new potential therapeutic target in CRC.
Highlights
A decrease in miR-203 expression[19,20,21]
The results showed that miR-203 expression was significantly lower in Colorectal cancer (CRC) tumor tissues compared to adjacent non-tumor tissues (Fig. 1A)
A reduction in the levels of miR-203 in the primary tumors with metastasis was noted compared to the primary tumors without metastasis (P < 0.05) (Fig. 1B), which suggested that the downregulation of miR-203 was closely related to the increase of CRC metastasis
Summary
A decrease in miR-203 expression[19,20,21]. Previous reports suggest that miR-203 plays a role in chemoresistance via downregulation of Akt[2] gene expression, which is implicated in the expression of the MTDH and HSP90 genes[22]. The molecular mechanisms of miR-203 in colorectal cancer remain largely unclear. There are reports depicting the expression and oncogenic role of EIF5A2 in hepatocellular carcinoma, and EIF5A2 has been suggested to modulate several pathophysiological processes by promoting cell proliferation and cell metastasis by inducing epithelial-mesenchymal transition (EMT)[24,25]. Zhu et al studied clinical samples from CRC patients and found that EIF5A2 might be involved in CRC aggressiveness and that EIF5A2 increased the expression of MTA1 to induce EMT26. We found that reduced expression of miR-203 in CRC is important in the acquisition of an aggressive and poor prognostic phenotype. The molecular mechanism of miR-203 involving in functional target was addressed in this study
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