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Article

microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma

Retraction in: /10.3892/or.2023.8660
  • Authors:
    • Zhaoxiang Yu
    • Xiaobo Lin
    • Ming Tian
    • Weiping Chang
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, The First Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710077, P.R. China
  • Pages: 731-738
    |
    Published online on: December 4, 2017
       https://doi.org/10.3892/or.2017.6130
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Abstract

Accumulating evidence indicates that microRNAs (miRNAs) play important roles in tumorigenesis and metastasis. Recent research has shown that miR‑196b is implicated in metastasis by regulating the migration and invasion of cancer cells. However, the clinical significance of miR‑196b and its role as well as the underlying mechanisms in hepatocellular carcinoma (HCC) remain largely unknown. Here, we detected miR‑196b expression in HCC and matched non-tumor tissues with qRT‑PCR. We found that miR‑196b displayed higher expression in HCC patient tissues and cells. Clinical analysis revealed that high miR‑196 expression was correlated with venous infiltration, advanced TNM stage and poor prognosis. Functionally, we demonstrated that miR‑196b promoted the migration and invasion of HCC cells in vitro. Moreover, miR‑196b knockdown restrained pulmonary metastasis in vivo. Mechanistically, we confirmed that miR‑196b could directly bind to 3'UTR of forkhead box P2 (FOXP2) mRNA and repress its expression. miR‑196b and FOXP2 showed a negative correlation in HCC tissues. More importantly, upregulation of FOXP2 antagonized miR‑196b‑mediated migration and invasion in Hep3B cells. Furthermore, FOXP2 knockdown partially reversed the anti‑metastatic function of the miR‑196b inhibitor on HCCLM3 cells. Taken together, we demonstrated that miR‑196b may function as a prognostic biomarker and suppressed FOXP2 expression, subsequently leading to the metastasis of HCC. Our findings highlight a novel mechanism of miR‑196b in the progression of HCC and identify miR‑196b/FOXP2 axis as a promising target for HCC.
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Copy and paste a formatted citation
Spandidos Publications style
Yu Z, Lin X, Tian M and Chang W: microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660. Oncol Rep 39: 731-738, 2018.
APA
Yu, Z., Lin, X., Tian, M., & Chang, W. (2018). microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660. Oncology Reports, 39, 731-738. https://doi.org/10.3892/or.2017.6130
MLA
Yu, Z., Lin, X., Tian, M., Chang, W."microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660". Oncology Reports 39.2 (2018): 731-738.
Chicago
Yu, Z., Lin, X., Tian, M., Chang, W."microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660". Oncology Reports 39, no. 2 (2018): 731-738. https://doi.org/10.3892/or.2017.6130
Copy and paste a formatted citation
x
Spandidos Publications style
Yu Z, Lin X, Tian M and Chang W: microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660. Oncol Rep 39: 731-738, 2018.
APA
Yu, Z., Lin, X., Tian, M., & Chang, W. (2018). microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660. Oncology Reports, 39, 731-738. https://doi.org/10.3892/or.2017.6130
MLA
Yu, Z., Lin, X., Tian, M., Chang, W."microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660". Oncology Reports 39.2 (2018): 731-738.
Chicago
Yu, Z., Lin, X., Tian, M., Chang, W."microRNA‑196b promotes cell migration and invasion by targeting FOXP2 in hepatocellular carcinoma Retraction in /10.3892/or.2023.8660". Oncology Reports 39, no. 2 (2018): 731-738. https://doi.org/10.3892/or.2017.6130
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