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miR-26a-5p suppresses tumor metastasis by regulating EMT and is associated with prognosis in HCC

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Abstract

Objective

To determine the role of miR-26a-5p in tumor invasion and metastasis in hepatocellular carcinoma (HCC).

Methods

We evaluated miR-26a-5p expression in HCC tissues by quantitative PCR and then analyzed its clinical significance using a Cox regression model. Transwell and nude mouse models were used to examine tumor metastasis in vitro and in vivo, respectively. The relationship between miR-26a-5p and epithelial-mesenchymal transition was also investigated by q-PCR and western blot.

Results

Strong downregulation of miR-26a-5p was observed in tumor tissues compared to paired adjacent normal tissues. Moreover, patients with low miR-26a-5p expression had a significantly poorer prognosis than those with high expression. The multivariate analysis indicated that miR-26a-5p expression was an independent prognostic indicator. The experimental transwell model and athymic mouse model revealed that miR-26a-5p depressed tumor metastasis in vitro and in vivo, respectively. In addition, the decreased miR-26a-5p level observed in HCC was associated with reduced E-cadherin expression and upregulation of vimentin, which affects the molecular mechanism of EMT.

Conclusion

Downregulation of miR-26a-5p promotes tumor metastasis by targeting EMT and influences the prognosis of HCC patients. Therefore, miR-26a-5p has potential as a new biomarker and therapeutic target.

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Correspondence to T. Guo.

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The authors have declared that no competing interests exist.

Ethical statement

This study was approved by the Research Ethics Committee of Zhongnan Hospital of Wuhan University. The study was conducted in full accordance with the 1964 Declaration of Helsinki and its later amendments. Informed consent was obtained from all individual participants included in the study.

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Chang, L., Li, K. & Guo, T. miR-26a-5p suppresses tumor metastasis by regulating EMT and is associated with prognosis in HCC. Clin Transl Oncol 19, 695–703 (2017). https://doi.org/10.1007/s12094-016-1582-1

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  • DOI: https://doi.org/10.1007/s12094-016-1582-1

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