Inhibition of Cell Proliferation and Metastasis by Scutellarein Regulating PI3K/Akt/NF-κB Signaling through PTEN Activation in Hepatocellular Carcinoma.
Sang Eun HaSeong Min KimPreethi VetrivelHun Hwan KimPritam Bhangwan BhosaleJeong Doo HeoJeong Doo HeoGon Sup KimPublished in: International journal of molecular sciences (2021)
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 μM concentration of SCU, three low-toxic concentrations of (25, 50, and 100) μM 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-κB 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-κB signaling by upregulation of PTEN, suggesting that SCU might be used as a potential agent for HCC therapy.
Keyphrases
- pi k akt
- signaling pathway
- cell cycle arrest
- cell proliferation
- poor prognosis
- epithelial mesenchymal transition
- long non coding rna
- induced apoptosis
- cell migration
- end stage renal disease
- cell cycle
- endothelial cells
- chronic kidney disease
- ejection fraction
- newly diagnosed
- stem cells
- papillary thyroid
- transcription factor
- prognostic factors
- immune response
- young adults
- high glucose
- type diabetes
- cell death
- binding protein
- bone marrow
- nuclear factor
- insulin resistance
- squamous cell carcinoma
- skeletal muscle
- replacement therapy
- patient reported outcomes