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BCL-XL overexpression promotes tumor progression-associated properties
Daniela Trisciuoglio1,2, Maria Grazia Tupone1, Marianna Desideri1
1Preclinical Models and New Therapeutic Agents Unit, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy.
Cell Death & Disease
|December 15, 2017
Summary
The anti-apoptotic protein BCL-XL fuels aggressive traits in melanoma and glioblastoma. Targeting BCL-XL may offer new therapeutic strategies for these challenging cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The protein BCL-XL is known to play a role in cell survival.
- Its specific contribution to the aggressive characteristics of melanoma and glioblastoma remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of BCL-XL in promoting aggressive features of human melanoma and glioblastoma.
- To determine if BCL-XL influences cancer stem cell phenotypes and vasculogenic mimicry.
Main Methods:
- Utilized human melanoma and glioblastoma cell lines with BCL-XL overexpression.
- Employed siRNA to reduce BCL-XL expression and a specific BCL-XL inhibitor.
- Analyzed in vitro cell migration, invasion, tumor sphere formation, stem cell markers, and in vivo xenograft models.
Main Results:
- BCL-XL overexpression enhanced melanoma and glioblastoma cell migration, invasion, and vasculogenic structure formation in vitro.
- BCL-XL-overexpressing cells showed increased tumor sphere formation and elevated stem cell marker levels, indicating a role in cancer stemness.
- Reduction of BCL-XL expression or inhibition of its activity counteracted these aggressive properties.
- Vasculogenic mimicry and vascular markers were upregulated in BCL-XL-overexpressing xenografts.
Conclusions:
- BCL-XL significantly contributes to the aggressive phenotype of melanoma and glioblastoma.
- BCL-XL plays a crucial role in maintaining cancer stem cell properties.
- Targeting BCL-XL presents a potential therapeutic strategy for aggressive melanoma and glioblastoma.
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