Novel synthetic chalcones induces apoptosis in human glioblastoma cells
Lucas Felipe Fernandes Bittencourt1, Karen Andrinéia de Oliveira2, Carine Bropp Cardoso1
1Laboratório de Biologia de Gliomas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Trindade, CEP: 88040-900, Florianópolis, SC, Brazil.
Abstract:
Glioblastoma multiforme is the main and most frequent tumor in adults' central nervous system. With a survival average of 5% two years after diagnosis, this type of cancer is a main health problem. Substances like the chalcones have been tested in order to develop new treatments. Here, we studied the effects of three synthetic chalcones (A23, C31 and J11) on A172 and surgery obtained-glioma cells. All chalcones showed a decrease in cell viability, mainly C31. An increase in apoptosis levels with no further increase of necrosis was observed. This augmentation may be linked to the high oxidative effect found, caused by the increased presence of reactive oxygen species and nitric oxide production. Cell cycle distribution showed an arrest at G0/G1 and S phases, suggesting that C31 interferes in cell cycle control. Our results shall aid in directing future research with this substance and its antitumor effect.
Insights
Synthetic chalcones show promise against glioblastoma multiforme, a deadly brain cancer. Chalcone C31 significantly reduced cancer cell viability and induced apoptosis, offering a potential new therapeutic avenue.
Area of Science:
- Neuro-oncology
- Pharmacology
Background:
- Glioblastoma multiforme is a prevalent and aggressive adult central nervous system tumor with a poor prognosis.
- Existing treatments for glioblastoma multiforme have limited efficacy, necessitating the development of novel therapeutic strategies.
Purpose of the Study:
- To investigate the antitumor effects of three synthetic chalcones (A23, C31, and J11) on glioblastoma cells.
- To evaluate the impact of these chalcones on cell viability, apoptosis, necrosis, oxidative stress, and cell cycle progression.
Main Methods:
- Treatment of A172 and primary glioma cells with synthetic chalcones A23, C31, and J11.
- Assessment of cell viability using standard assays.
- Analysis of apoptosis and necrosis induction.
- Measurement of reactive oxygen species (ROS) and nitric oxide (NO) production.
- Flow cytometry to determine cell cycle distribution.
Main Results:
- All tested chalcones reduced glioblastoma cell viability, with C31 exhibiting the most significant effect.
- Chalcones increased apoptosis levels without a corresponding increase in necrosis.
- Elevated levels of ROS and NO were observed, suggesting an oxidative stress mechanism.
- Chalcone C31 induced cell cycle arrest at the G0/G1 and S phases.
Conclusions:
- Synthetic chalcones, particularly C31, demonstrate significant cytotoxic and pro-apoptotic effects on glioblastoma cells.
- The observed antitumor activity is potentially mediated by oxidative stress and cell cycle disruption.
- These findings support further investigation of C31 as a potential therapeutic agent for glioblastoma treatment.
