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Article

JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway

  • Authors:
    • Bufei Zhao
    • Ting Hu
  • View Affiliations / Copyright

    Affiliations: Department of Hepatopancreatobiliary Surgery, Affiliated Hospital of Beihua University, Jilin 132001, P.R. China, Department of Oncology, The First Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China
  • Pages: 1939-1945
    |
    Published online on: November 30, 2018
       https://doi.org/10.3892/ol.2018.9780
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Abstract

The increased worldwide mortality rate due to liver cancer may be attributed to the aggressive nature of the disease. Signal transduction through G‑protein‑coupled receptors (GPCRs) can affect a number of aspects of cancer biology, including invasion, migration and vascular remodelling. JTC‑801, a novel GPCR antagonist, has demonstrated promising anticancer effects in adenocarcinoma and osteosarcoma cells. In the present study, the effect of JTC‑801 on the proliferation and migration of hepatoblastoma Hep G2 cells was investigated. The Cell Counting Kit‑8 assay revealed that JTC‑801 markedly suppressed the growth of the Hep G2 cells. Additionally, JTC‑801 significantly inhibited cell invasion and migration in a Transwell assay. Furthermore, the expression of anti‑apoptotic protein B‑cell lymphoma 2 decreased and the expression of the pro‑apoptotic proteins active caspase‑3 and apoptosis regulator BAX increased in the Hep G2 cells following JTC‑801 treatment. Additionally, JTC‑801 suppressed the phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT) signalling pathway in the Hep G2 cells. Therefore, the present study revealed that JTC‑801 can induce the apoptosis of Hep G2 cells by regulating the PI3K/AKT signalling pathway, which suggests that JTC‑801 may be a potential novel drug target for clinical liver cancer treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Zhao B and Hu T: JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway. Oncol Lett 17: 1939-1945, 2019.
APA
Zhao, B., & Hu, T. (2019). JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway. Oncology Letters, 17, 1939-1945. https://doi.org/10.3892/ol.2018.9780
MLA
Zhao, B., Hu, T."JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway". Oncology Letters 17.2 (2019): 1939-1945.
Chicago
Zhao, B., Hu, T."JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway". Oncology Letters 17, no. 2 (2019): 1939-1945. https://doi.org/10.3892/ol.2018.9780
Copy and paste a formatted citation
x
Spandidos Publications style
Zhao B and Hu T: JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway. Oncol Lett 17: 1939-1945, 2019.
APA
Zhao, B., & Hu, T. (2019). JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway. Oncology Letters, 17, 1939-1945. https://doi.org/10.3892/ol.2018.9780
MLA
Zhao, B., Hu, T."JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway". Oncology Letters 17.2 (2019): 1939-1945.
Chicago
Zhao, B., Hu, T."JTC‑801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3‑kinase/protein kinase B signalling pathway". Oncology Letters 17, no. 2 (2019): 1939-1945. https://doi.org/10.3892/ol.2018.9780
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