4.7 Article

Inhibition of Cell Proliferation and Metastasis by Scutellarein Regulating PI3K/Akt/NF-κB Signaling through PTEN Activation in Hepatocellular Carcinoma

Journal

Publisher

MDPI
DOI: 10.3390/ijms22168841

Keywords

scutellarein; proliferation; metastasis; PTEN; PI3K/Akt/NF-kappa B; EMT

Funding

  1. National Research Foundation of Korea - Ministry of Science and ICT [2020R1A2B5B01001807]
  2. National Research Foundation of Korea [2020R1A2B5B01001807] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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SCU as a potential agent for HCC therapy inhibits cell proliferation and metastasis in HepG2 cells through upregulation of PTEN and inhibition of the PI3K/Akt/NF-kappa B signaling pathway. It is a natural based agent that shows promise in improving therapeutic outcomes for HCC treatment.
Scutellarein (SCU) is a well-known flavone with a broad range of biological activities against several cancers. Human hepatocellular carcinoma (HCC) is major cancer type due to its poor prognosis even after treatment with chemotherapeutic drugs, which causes a variety of side effects in patients. Therefore, efforts have been made to develop effective biomarkers in the treatment of HCC in order to improve therapeutic outcomes using natural based agents. The current study used SCU as a treatment approach against HCC using the HepG2 cell line. Based on the cell viability assessment up to a 200 mu M concentration of SCU, three low-toxic concentrations of (25, 50, and 100) mu M were adopted for further investigation. SCU induced cell cycle arrest at the G2/M phase and inhibited cell migration and proliferation in HepG2 cells in a dose-dependent manner. Furthermore, increased PTEN expression by SCU led to the subsequent downregulation of PI3K/Akt/NF-kappa B signaling pathway related proteins. In addition, SCU regulated the metastasis with EMT and migration-related proteins in HepG2 cells. In summary, SCU inhibits cell proliferation and metastasis in HepG2 cells through PI3K/Akt/NF-kappa B signaling by upregulation of PTEN, suggesting that SCU might be used as a potential agent for HCC therapy.

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