{Reference Type}: Journal Article
{Title}: Carnosol Inhibits the Proliferation, Migration, and Invasion of Hepatocellular Carcinoma Cells in vitro by Regulating the AMPK Signaling Pathway.
{Author}: Kong S;Xiao W;Ma T;Chen Y;Shi H;Tu J;Zou J;Zhang M;
{Journal}: Anticancer Agents Med Chem
{Volume}: 0
{Issue}: 0
{Year}: 2023 04 18
{Factor}: 2.527
{DOI}: 10.2174/1871520623666230418093254
{Abstract}: Hepatocellular carcinoma (HCC) is one of the most malignant cancers in the world, and its 5-
year survival rate is low. At present, for advanced primary liver cancer, the clinical treatment often adopts the systemic
method, but there is no effective targeted treatment. The average survival time of patients with liver cancer after drug
treatment is only 3-5 months. Therefore, it is of great clinical significance to find new and effective drugs for the
treatment of HCC. Carnosol (CA) is a bioactive diterpene compound present in Lamiaceae spp., which has been
demonstrated to have antioxidant, anti-inflammatory, and anticancer properties.
In this study, we aimed to reveal the effect of carnosol on HCC and provide new possibilities for the drug therapy
of HCC.
The objective of this study is to observe the effect of carnosol on the tumor phenotype and signaling pathway
of HCC cells.
We treated two different human HCC cells, HepG2 and Huh7, with carnosol. The cells were analyzed using
the CCK-8 assay for viability and proliferation. The cell migration and invasion were detected by Transwell assay. The
molecular markers of cell proliferation, apoptosis, migration, invasion, and signaling pathways were detected by RTPCR
and WB. In addition, we performed rescue experiments with inhibitors to verify the affected signaling pathway.
The results showed that carnosol could significantly inhibit HCC cell viability, effort, colony formation, migration,
and invasion. Moreover, Carnosol promoted the apoptosis of HCC cells. Mechanically, carnosol activated the
AMPK-p53 pathway.
To conclude, our study demonstrated that carnosol could inhibit proliferation, migration, invasion, and
promote apoptosis via activating AMPK-p53 in HCC cells.