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Dianhydrogalactitol, a potential multitarget agent, inhibits glioblastoma migration, invasion, and angiogenesis
Xia Jiang1, Yinmei Huang1, Xiaojie Wang2
1The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
Abstract:
The complexity of cancer has led to single-target agents exhibiting lower-than-desired clinical efficacy. Drugs with multiple targets provide a feasible option for the treatment of complex tumors. Multitarget anti-angiogenesis agents are among the new generation of anticancer drugs and have shown favorable clinical efficacy. Dianhydrogalactitol (DAG) is a chemotherapeutic agent for chronic myeloid leukemia and lung cancer. Recently, it has been tested in phase II trials of glioblastoma treatment; however, mechanisms of DAG in glioblastoma have not been elucidated. Here we show that DAG could inhibit the migration and invasion of U251 cell line by inhibiting matrix metalloproteinase-2 (MMP2) expression. Furthermore, DAG could also inhibit tumor angiogenesis in vitro as well as in the zebrafish model. Mechanistic studies reveal that DAG inhibited both VEGFR2 and FGFR1 pathways. Our results suggest that DAG may be a potential multitarget agent that can inhibit tumor migration, invasion, and angiogenesis, and the anti-angiogenic effects may be involved in dual-suppression VEGF/VEGFR2 and FGF2/FGFR1 signal pathways.
Insights
Dianhydrogalactitol (DAG) inhibits glioblastoma cell migration, invasion, and angiogenesis by targeting multiple pathways. This multitarget approach shows promise for treating complex tumors like glioblastoma.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Single-target cancer agents show limited efficacy against complex tumors.
- Multitarget agents offer a promising strategy for cancer treatment.
- Dianhydrogalactitol (DAG) is an anticancer drug with potential in glioblastoma therapy, but its mechanisms are unclear.
Purpose of the Study:
- To investigate the mechanisms of Dianhydrogalactitol (DAG) in glioblastoma.
- To evaluate DAG's potential as a multitarget anti-angiogenesis agent.
Main Methods:
- In vitro studies using U251 glioblastoma cell line.
- In vitro and zebrafish model studies for angiogenesis.
- Analysis of matrix metalloproteinase-2 (MMP2) expression.
- Investigation of VEGFR2 and FGFR1 signaling pathways.
Main Results:
- DAG inhibited U251 cell migration and invasion by reducing MMP2 expression.
- DAG demonstrated anti-angiogenic effects in vitro and in vivo.
- DAG suppressed both VEGFR2 and FGFR1 signaling pathways.
Conclusions:
- DAG acts as a multitarget agent inhibiting glioblastoma cell migration, invasion, and angiogenesis.
- DAG's anti-angiogenic effects are mediated by dual suppression of VEGF/VEGFR2 and FGF2/FGFR1 pathways.
- DAG shows potential as a novel therapeutic agent for glioblastoma.
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