Parthenolide-induced apoptosis, autophagy and suppression of proliferation in HepG2 cells
Jing Sun1, Chan Zhang, Yong-Li Bao
1National Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun, China E-mail : baoyl1967@163.com, liyx486@nenu.edu.cn.
Purpose:
To investigate the anticancer effects and underlying mechanisms of parthenolide on HepG2 human hepatocellular carcinoma cells.
Materials And Methods:
Cell viability was assessed by MTT assay and cell apoptosis through DAPI, TUNEL staining and Western blotting. Monodansylcadaverin(MDC) and AO staining were used to detect cell autophagy. Cell proliferation was assessed by Ki67 immunofluorescence staining.
Results:
Parthenolide induced growth inhibition in HepG2 cells. DAPI and TUNEL staining showed that parthenolide could increase the number of apoptotic nuclei, while reducing the expression of the anti-apoptotic protein Bcl-2 and elevating the expression of related proteins, like p53, Bax, cleaved caspase9 and cleaved caspase3. Parthenolide could induce autophagy in HepG2 cells and inhibited the expression of proliferation-related gene, Ki-67.
Conclusions:
Parthenolide can exert anti-cancer effects by inducing cell apoptosis, activating autophagy and inhibiting cell proliferation.
Insights
Parthenolide, a natural compound, demonstrated significant anticancer effects against HepG2 liver cancer cells by inducing apoptosis, activating autophagy, and inhibiting cell proliferation, offering potential therapeutic strategies.
Area of Science:
- Hepatocellular carcinoma research
- Natural product pharmacology
- Cellular mechanisms of cancer
Background:
- Hepatocellular carcinoma (HCC) remains a significant global health challenge.
- Parthenolide, a sesquiterpene lactone, has shown potential anticancer properties.
- Understanding parthenolide's mechanisms in HCC is crucial for therapeutic development.
Purpose of the Study:
- To investigate the anticancer effects of parthenolide on HepG2 human hepatocellular carcinoma cells.
- To elucidate the underlying molecular mechanisms of parthenolide's action.
- To evaluate parthenolide's impact on cell viability, apoptosis, autophagy, and proliferation.
Main Methods:
- Cell viability assessed using MTT assay.
- Apoptosis evaluated via DAPI, TUNEL staining, and Western blotting.
- Autophagy detected by MDC and AO staining; proliferation assessed by Ki67 staining.
Main Results:
- Parthenolide significantly inhibited HepG2 cell growth.
- Induced apoptosis was evidenced by increased apoptotic nuclei and altered expression of apoptosis-related proteins (p53, Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3).
- Parthenolide treatment activated autophagy and suppressed proliferation marker Ki-67.
Conclusions:
- Parthenolide exhibits potent anticancer activity against HepG2 cells.
- Mechanisms involve induction of apoptosis, activation of autophagy, and inhibition of cell proliferation.
- Parthenolide represents a promising candidate for HCC therapy.
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