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Effect on cell cycle progression by N-Myc knockdown in SK-N-BE(2) neuroblastoma cell line and cytotoxicity with
Un-Young Yu1, Je-Eun Cha, Sun-Young Ju
1Department of Microbiology, Ewha Womans University School of Medicine, Seoul, Korea.
Purpose:
Neuroblastoma is a common tumor in childhood, and generally exhibits heterogeneity and a malignant progression. MYCN expression and amplification profiles frequently correlate with therapeutic prognosis. Although it has been reported that MYCN silencing causes differentiation and apoptosis in human neuroblastoma cells, MYCN expression influences the cytotoxic potential of chemotherapeutic drugs via the deregulation of the cell cycle. STI-571 may constitute a promising therapeutic agent against neuroblastoma, particularly in cases in which c-Kit is expressed preferentially in MYCN-amplified neuroblastoma.
Materials And Methods:
To determine whether STI-571 exerts a synergistic effect on cytotoxicity with MYCN expression, we assessed apoptotic cell death and cell cycle distribution after 72 h of exposure to STI-571 with or with out treatment of SK-N-BE(2) neuroblastoma cells with MYCN siRNA.
Results:
MYCN siRNA-treated SK-N-BE(2) cells did not affect apoptosis and cells were arrested in G0/G1 phase after STI-571 treatment.
Conclusions:
siRNA therapy targeted to MYCN may not be effective when administered in combination with STI-571 treatment in cases of neuroblastoma. Therefore, chemotherapeutic drugs that target S or G2-M phase may prove ineffective when applied to cells arrested in the G0/1 phase as the result of MYCN knockdown and STI-571 treatment.
Insights
MYCN silencing combined with STI-571 treatment did not enhance neuroblastoma cell death. This combination therapy may be ineffective due to cell cycle arrest in the G0/G1 phase.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Neuroblastoma is a heterogeneous childhood cancer with malignant potential.
- MYCN expression is a key prognostic indicator in neuroblastoma.
- MYCN influences chemotherapy response by deregulating the cell cycle.
Purpose of the Study:
- To investigate the synergistic effect of STI-571 and MYCN silencing on neuroblastoma cell cytotoxicity.
- To assess the impact of MYCN knockdown on neuroblastoma cell apoptosis and cell cycle distribution when treated with STI-571.
Main Methods:
- SK-N-BE(2) neuroblastoma cells were treated with MYCN siRNA and STI-571.
- Apoptotic cell death and cell cycle distribution were analyzed after 72 hours of exposure.
Main Results:
- MYCN siRNA treatment alone did not significantly affect apoptosis.
- STI-571 treatment resulted in cell cycle arrest at the G0/G1 phase.
- The combination of MYCN siRNA and STI-571 did not enhance apoptotic cell death.
Conclusions:
- Combined MYCN siRNA and STI-571 therapy may not be effective for neuroblastoma treatment.
- Chemotherapeutic agents targeting S or G2-M phases may be ineffective in MYCN-knockdown neuroblastoma cells arrested in G0/G1 phase.
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