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Original Abstract of the Article :
OBJECTIVE: To investigate the new mechanism of temozolomide (TMZ) induced anti-tumor effects on glioblastoma cells in vitro. METHODS: Grade IV glioma cell lines SHG44 and U251 cells were treated with TMZ. MTT test was used to determine the proliferation of glioma cells. Hoechst 33342 assay was used...See full text at original site
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引用元:
https://doi.org/10.3760/cma.j.issn.0253-3766.2012.10.004
データ提供:米国国立医学図書館(NLM)
Temozolomide's Anti-Tumor Effects: A New Mechanism Unveiled
Glioblastoma, a brain tumor known for its aggressive nature, is like a desert mirage, posing a significant challenge to medical professionals. Temozolomide (TMZ), a chemotherapy drug, has been used to fight this formidable foe, but its precise mechanism of action has remained somewhat elusive. This study, like a meticulous explorer uncovering hidden secrets, seeks to unravel the complex mechanisms underlying TMZ's anti-tumor effects on glioblastoma cells in the lab. Researchers carefully tested TMZ on glioblastoma cell lines, observing the effects of the drug on cell growth, apoptosis (programmed cell death), and cell cycle progression. They also delved into the role of reactive oxygen species (ROS), a type of molecule known to play a role in cell signaling.Temozolomide's Anti-Tumor Effects: A New Mechanism Unveiled
The study revealed that TMZ effectively inhibited the growth of glioblastoma cells, inducing apoptosis and arresting cell cycle progression. Importantly, the researchers discovered that TMZ's anti-tumor effects were mediated through a specific pathway involving ROS and SIRT1, a protein known to play a role in cellular aging and stress response.Temozolomide's Anti-Tumor Effects: A New Mechanism Unveiled
This study provides valuable insights into the complex interactions between TMZ, ROS, and SIRT1 in glioblastoma cells.Dr.Camel's Conclusion
This study uncovers a new mechanism by which temozolomide exerts its anti-tumor effects on glioblastoma cells.Date :
- Date Completed 2013-07-11
- Date Revised 2018-12-02
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