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Aberrant expression of miR-199a-3p and its clinical significance in colorectal cancers

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Abstract

Aberrant miR-199a-3p expression has been reported in several cancers. However, the clinical significance of miR-199a-3p in human colorectal cancer has not been addressed. In this study, we detected miR-199a-3p expression in 92 colorectal cancer cases to evaluate its clinicopathologic characteristics in colorectal cancer. We showed that miR-199a-3p expression was significantly upregulated in cancer tissues than NATs. Clinicopathologic analysis revealed that high miR-199a-3p expression contributed to more advanced lymphatic invasion, lymph node metastasis, liver metastases and late TNM stage in colorectal cancer. Kaplan–Meier analysis showed that high expression of miR-199a-3p could lead to a significantly shorter overall survival rate. Cox’s proportional hazards model also indicated that the high expression of miR-199a-3p could serve as an independent and significant prognostic factor for survival. We transfected miR-199a-3p inhibitor into SW480 cells and observed that miR-199a-3p inhibitor could markedly inhibit the cell proliferation. Flow cytometry analysis also found that miR-199a-3p inhibitor could cause G0/G1 arrest, decreased percentage of S and G2/M phase and induce more cell apoptosis in SW480 cells. These results suggested that miR-199a-3p may serve as an efficient biomarker for diagnosis and novel prognostic indicator in colorectal cancer.

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Acknowledgments

This work was supported by grants from Medical Science and Technology Development Foundation, Jiangsu Province Department of Health (No. H201013 and H201209), National Natural Science Foundation of China (No. 81130057 and 81201905) and Nature Science Research Grants in University of Jiangsu Province of P.R. China (No. 12KJB320009).

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Correspondence to Qiaoming Zhi or Liang Wang.

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Daiwei Wan and Songbing He contributed equally to this work.

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Wan, D., He, S., Xie, B. et al. Aberrant expression of miR-199a-3p and its clinical significance in colorectal cancers. Med Oncol 30, 378 (2013). https://doi.org/10.1007/s12032-012-0378-6

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  • DOI: https://doi.org/10.1007/s12032-012-0378-6

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