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miR-93 enhances hepatocellular carcinoma invasion and metastasis by EMT via targeting PDCD4

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Abstract

Objectives

To clarify the potential biological function of miR-93 and its related molecular mechanism underlying metastasis in human hepatocellular carcinoma (HCC).

Results

miR-93 was significantly up-regulated in HCC tissues and was associated with poor 5-year overall survival in HCC patients. Transwell assays showed that over-expression of miR-93 increased HCC cell migration and invasion in vitro. Programmed cell death 4 (PDCD4) was a target gene of miR-93 and miR-93 could down-regulate the expression of PDCD4 by directly targeting its 3′-UTR. The re-expression of PDCD4 could attenuate the HCC cell invasion and migration induced by miR-93, while the knockdown of PDCD4 would promote HCC cell migration and invasion via the epithelial-mesenchymal transition (EMT) pathway.

Conclusions

miR-93 provides new insight into the molecular mechanisms of pathogenesis and progression in HCC and offer a potential therapeutic target for the treatment of HCC patients.

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Authors and Affiliations

  1. Department of Clinical Laboratory, People’s Hospital of Weifang, Weifang, Shandong, People’s Republic of China

    Chunmei Ji

  2. Department of Interventional Therapy, Yidu Central Hospital of Weifang, Weifang, Shandong, People’s Republic of China

    Hang Liu

  3. Department of Oncology, People‘s Hospital of Rizhao, Rizhao, Shandong, People’s Republic of China

    Qiang Yin

  4. Department of PIVAS, People’s Hospital of Zhangqiu, Jinan, Shandong, People’s Republic of China

    Hui Li

  5. Department of Pathology, Qingdao Municipal Hospital, No. 1 Jiaozhou Road, Shibei District, Qingdao, 266000, Shandong, People’s Republic of China

    Han Gao

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  1. Chunmei Ji
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  2. Hang Liu
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  3. Qiang Yin
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  4. Hui Li
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  5. Han Gao
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Correspondence to Han Gao.

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Ji, C., Liu, H., Yin, Q. et al. miR-93 enhances hepatocellular carcinoma invasion and metastasis by EMT via targeting PDCD4. Biotechnol Lett 39, 1621–1629 (2017). https://doi.org/10.1007/s10529-017-2403-5

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  • DOI: https://doi.org/10.1007/s10529-017-2403-5

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