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Ganoderic acid A inhibits proliferation and invasion, and promotes apoptosis in human hepatocellular carcinoma cells
Xu Wang1, Di Sun1, Jiandong Tai1
1Department of Colorectal and Anal Surgery, The First Hospital, Jilin University, Changchun, Jilin 130000, P.R. China.
Abstract:
Ganoderic acid A (GA‑A), a triterpenoid, has been demonstrated to suppress cell proliferation in various cancers, including breast cancer and osteosarcoma. However, its effect on human hepatocellular carcinoma (HCC) remains to be elucidated. The present study aimed to investigate the effect of GA‑A on HCC cells in vitro. The HepG2 and SMMC7721 human HCC cell lines were treated with differing concentrations of GA‑A for 24, 48 and 72 h. The cell growth rate, cell cycle and apoptosis, migration and invasion were determined using a Cell Counting Kit‑8, flow cytometry and transwell assays, respectively. The expression of apoptosis‑associated proteins was detected via western blot analysis. GA‑A significantly inhibited the proliferation of human HCC HepG2 and SMMC7721 cells in a dose‑dependent manner. Furthermore, GA‑A induced cell cycle arrest at the G0/G1 phase and apoptosis, and suppressed the migration and invasion of HCC cells. Furthermore, GA‑A decreased the expression of cyclin D1 and increased the expression of p21 and cleaved caspase‑3. In conclusion, GA‑A suppressed the proliferation of human HCC cells in vitro and may act as a promising natural therapeutic reagent in the treatment of HCC.
Insights
Ganoderic acid A (GA-A) effectively suppresses human hepatocellular carcinoma (HCC) cell proliferation, migration, and invasion. This natural triterpenoid induces cell cycle arrest and apoptosis, showing promise as an anticancer therapeutic for HCC.
Area of Science:
- Pharmacology
- Oncology
- Molecular Biology
Background:
- Ganoderic acid A (GA-A), a triterpenoid, exhibits anticancer properties in various cancers.
- The therapeutic potential of GA-A in human hepatocellular carcinoma (HCC) requires further investigation.
Purpose of the Study:
- To investigate the in vitro effects of GA-A on human HCC cell lines.
- To determine GA-A's impact on HCC cell proliferation, cell cycle, apoptosis, migration, and invasion.
Main Methods:
- Human HCC cell lines (HepG2, SMMC7721) were treated with varying GA-A concentrations.
- Cell proliferation, cell cycle, apoptosis, migration, and invasion were assessed using CCK-8, flow cytometry, and Transwell assays.
- Apoptosis-associated protein expression was analyzed via Western blot.
Main Results:
- GA-A significantly inhibited HCC cell proliferation in a dose-dependent manner.
- GA-A induced G0/G1 cell cycle arrest and promoted apoptosis in HCC cells.
- GA-A suppressed HCC cell migration and invasion, decreasing cyclin D1 and increasing p21 and cleaved caspase-3 expression.
Conclusions:
- GA-A demonstrates potent inhibitory effects on human HCC cell proliferation, migration, and invasion in vitro.
- GA-A's mechanisms involve cell cycle arrest and induction of apoptosis.
- GA-A represents a potential natural therapeutic agent for HCC treatment.
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