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Selectively targeting BCL6 using a small-molecule inhibitor is a potential therapeutic strategy for glioblastoma
Min Wu1, Lin Zhang1, Weikai Guo1
1East China Normal University, Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, Shanghai 200241, China.
Abstract:
Glioblastoma multiforme (GBM) is the deadliest form of brain tumor, and effective treatments are lacking. Thus, a new generation of effective treatments is urgently needed. B-cell lymphoma 6 (BCL6) is a transcription factor that functions to suppress the transcription of DNA damage response genes, halting cell death in response to DNA damage. Here, we identified BCL6 as a lynchpin in GBM, the expression of which was greater in GBM cells than in normal cells and associated with poor survival in GBM patients. The silencing of BCL6 additionally affected GBM cell proliferation and triggered cellular damage. Furthermore, we reported the identification of YK01, a novel small-molecule inhibitor of BCL6. YK01 exhibited excellent anti-GBM bioactivity and caused apoptosis; importantly, YK01 significantly inhibited the growth of GBM cells both in vitro and in vivo. Moreover, the combination of YK01 and temozolomide treatment significantly suppressed the growth and metastasis of tumors in vivo and prolonged the survival of mice with tumors. In summary, our findings reveal that BCL6 appears to play a crucial role in GBM and may be a therapeutic target for treating this incurable condition.
Insights
B-cell lymphoma 6 (BCL6) is crucial in glioblastoma multiforme (GBM), a deadly brain tumor. Targeting BCL6 with the novel inhibitor YK01 shows promise for new GBM treatments.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Glioblastoma multiforme (GBM) is an aggressive brain tumor with limited treatment options.
- B-cell lymphoma 6 (BCL6) is a transcription factor that inhibits DNA damage response, promoting cancer cell survival.
- Elevated BCL6 expression is linked to poor prognosis in GBM patients.
Purpose of the Study:
- To investigate the role of BCL6 in GBM pathogenesis.
- To identify and evaluate novel therapeutic strategies targeting BCL6 for GBM treatment.
Main Methods:
- Analysis of BCL6 expression in GBM patient samples.
- In vitro and in vivo studies using GBM cell lines and mouse models.
- Development and testing of YK01, a small-molecule BCL6 inhibitor.
- Combination therapy studies with YK01 and temozolomide.
Main Results:
- BCL6 expression is upregulated in GBM and correlates with reduced patient survival.
- Silencing BCL6 inhibits GBM cell proliferation and induces DNA damage.
- YK01 effectively inhibits GBM cell growth in vitro and in vivo, inducing apoptosis.
- Combined YK01 and temozolomide treatment significantly suppresses tumor growth, metastasis, and prolongs survival in mice.
Conclusions:
- BCL6 is a critical factor in GBM development and progression.
- BCL6 represents a promising therapeutic target for glioblastoma.
- YK01 demonstrates significant anti-GBM activity and potential for combination therapy.
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