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JSI-124 inhibits glioblastoma multiforme cell proliferation through G(2)/M cell cycle arrest and apoptosis augment
Yuhang Su1, Gang Li, Xulong Zhang
1Department of Neurosurgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Abstract:
JSI-124 (cucurbitacin I) is a selective inhibitor of Janus kinase/signal transducer and activator of transcription 3(JAK/STAT3) and has been shown to exert anti-proliferative and anti-tumor properties both in vitro and in vivo. As STAT3 activation has been implicated in the development of glioma, we investigated the therapeutic efficacy of JSI-124 on glioblastoma multiforme (GBM) by interfering with STAT3 pathway. In present study, two GBM cell lines, U251 and A172 cells, were treated with JSI-124. The results showed that the cell growth was inhibited significantly in a dose-and time-dependent manner. Further investigation illustrated that the levels of phosphorylated-STAT3 were decreased in GBM cells treated by JSI-124, concomitant with apoptosis augment and cell cycle arrest. Specially, JSI-124 induced G(2)/M accumulation via downregulation of cyclin B1 and cdc2 expression. Together these results suggested that inhibition of STAT3 by JSI-124 is a potential strategy for the development of the new glioblastoma multiforme therapeutics.
Insights
JSI-124 effectively inhibits glioblastoma multiforme (GBM) cell growth by targeting the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway. This compound promotes apoptosis and cell cycle arrest, showing potential as a novel GBM therapeutic.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Signal transducer and activator of transcription 3 (STAT3) activation is implicated in glioma development.
- Glioblastoma multiforme (GBM) is an aggressive brain tumor with limited therapeutic options.
- Targeting the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway is a potential therapeutic strategy for GBM.
Purpose of the Study:
- To investigate the therapeutic efficacy of JSI-124 (cucurbitacin I) on glioblastoma multiforme (GBM) by interfering with the STAT3 pathway.
- To evaluate the effect of JSI-124 on GBM cell proliferation, apoptosis, and cell cycle.
- To determine the impact of JSI-124 on phosphorylated-STAT3 levels in GBM cells.
Main Methods:
- Treatment of U251 and A172 GBM cell lines with JSI-124.
- Assessment of cell growth inhibition using dose- and time-dependent assays.
- Analysis of phosphorylated-STAT3 levels.
- Evaluation of apoptosis induction and cell cycle arrest.
- Investigation of cyclin B1 and cdc2 expression changes.
Main Results:
- JSI-124 significantly inhibited GBM cell growth in a dose- and time-dependent manner.
- JSI-124 treatment led to decreased levels of phosphorylated-STAT3 in GBM cells.
- JSI-124 induced apoptosis and cell cycle arrest at the G2/M phase.
- Downregulation of cyclin B1 and cdc2 expression was observed following JSI-124 treatment.
Conclusions:
- JSI-124 demonstrates significant anti-proliferative and anti-tumor effects on GBM cells.
- Inhibition of the STAT3 pathway by JSI-124 is a promising therapeutic strategy for GBM.
- JSI-124 holds potential for the development of novel glioblastoma multiforme therapeutics.
