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Article Open Access

MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma

  • Authors:
    • Manya Wu
    • Chaoyuan Huang
    • Xinping Huang
    • Rong Liang
    • Yan Feng
    • Xiaoling Luo
  • View Affiliations / Copyright

    Affiliations: Research Department, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China, Department of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China, First Department of Chemotherapy, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China
    Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2173-2181
    |
    Published online on: August 11, 2017
       https://doi.org/10.3892/or.2017.5900
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Abstract

In our previous studies, the Illumine Soledad massively parallel signature sequencing of miRNomes in non‑tumor and hepatocellular carcinoma (HCC) tissues revealed that microRNA (miR)-144-3p was significantly downregulated in HCC, but its role in HCC development, especially angiogenesis, remains unclear. In this investigation, we found recovering miR‑144‑3p expression can significantly suppress the growth, migration and induced angiogenic capacity of HCC cells through both in vivo and in vitro experiments. Moreover, clinical correlation analysis showed that low expression of miR‑144‑3p was positively correlated to poor disease-free survival (DFS) of HCC patients. Mechanistically, serum and glucocorticoid kinase 3 (SGK3), the putative targets of miR‑144‑3p, was predicted by Target Scan database and identified to be suppressed by miR‑144‑3p so that inhibiting the activation of mTOR-VEGF downstream signals was activated by the phosphoinositide 3-kinase (PI3K)-independent pathway. Hence, we concluded that miR‑144‑3p, which is frequently downregulated in HCC, can inhibit proliferation, migration and repress angiogenesis by regulating SGK3 activation with PI3K independent signal pathway, and acts as a prognostic factor for HCC patients.
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Copy and paste a formatted citation
Spandidos Publications style
Wu M, Huang C, Huang X, Liang R, Feng Y and Luo X: MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma. Oncol Rep 38: 2173-2181, 2017.
APA
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., & Luo, X. (2017). MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma. Oncology Reports, 38, 2173-2181. https://doi.org/10.3892/or.2017.5900
MLA
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., Luo, X."MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma". Oncology Reports 38.4 (2017): 2173-2181.
Chicago
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., Luo, X."MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma". Oncology Reports 38, no. 4 (2017): 2173-2181. https://doi.org/10.3892/or.2017.5900
Copy and paste a formatted citation
x
Spandidos Publications style
Wu M, Huang C, Huang X, Liang R, Feng Y and Luo X: MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma. Oncol Rep 38: 2173-2181, 2017.
APA
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., & Luo, X. (2017). MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma. Oncology Reports, 38, 2173-2181. https://doi.org/10.3892/or.2017.5900
MLA
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., Luo, X."MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma". Oncology Reports 38.4 (2017): 2173-2181.
Chicago
Wu, M., Huang, C., Huang, X., Liang, R., Feng, Y., Luo, X."MicroRNA-144-3p suppresses tumor growth and angiogenesis by targeting SGK3 in hepatocellular carcinoma". Oncology Reports 38, no. 4 (2017): 2173-2181. https://doi.org/10.3892/or.2017.5900
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