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Updated: Jul 8, 2025
Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
Published on: April 22, 2017
REC8 regulates neuroblastoma cell proliferation, migration, invasion, and angiogenesis via STAT3/VEGF signaling
Qiang Wang1, Wei Fan2, ZengHui Hao2
1Department of Pediatric Surgery, The Sixth Affiliated Hospital of Harbin Medical University, Harbin, 150001, China. doctor_wang@vip.163.com.
Background:
Neuroblastoma, one of the most prevalent childhood cancers, is often treated with surgery, radiation, and chemotherapy. However, prognosis and survival are still dismal for children with neuroblastoma at high risk. Consequently, it is vital to identify new and effective treatment targets. As a component of the meiotic cohesion complex, REC8 is involved in a wide range of malignancies. The current work assessed the impact of REC8 knockdown on SH-SY5Y and SK-N-AS neuroblastoma cells and delved into the molecular mechanism behind this effect.
Methods:
Knockdown of REC8 using the small interfering (si) RNA technology, and the results were verified by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot. The Cell Counting Kit-8 (CCK-8) was used to examine cell proliferation, while flow cytometry was used to examine cell cycle progression and apoptosis. Analyses of angiogenesis included tube formation experiments. Transwell tests were used to examine cell migration and invasion.
Results:
The data showed that downregulation of the REC8 led to a substantial decrease in cell proliferation by stopping the cell cycle in the G1 phase. REC8 knockdown significantly reduced neuroblastoma cell proliferation, migration, invasion, angiogenesis, induced cell cycle arrest, and enhanced apoptosis. We also discovered that repressing REC8 expression in neuroblastoma cell lines SH-SY5Y and SK-N-AS reduced their ability to activate the STAT3/VEGF signaling pathway.
Conclusions:
Neuroblastoma therapy may benefit from targeting REC8 and its downstream targets.
Insights
Targeting REC8, a protein in the meiotic cohesion complex, significantly inhibits neuroblastoma growth, migration, and angiogenesis. Knocking down REC8 induces cell cycle arrest and apoptosis, offering a promising therapeutic strategy for high-risk neuroblastoma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Neuroblastoma is a prevalent childhood cancer with poor prognosis for high-risk cases.
- REC8, a component of the meiotic cohesion complex, is implicated in various malignancies.
- Identifying novel therapeutic targets is crucial for improving neuroblastoma treatment outcomes.
Purpose of the Study:
- To investigate the impact of REC8 knockdown on neuroblastoma cell lines (SH-SY5Y and SK-N-AS).
- To elucidate the molecular mechanisms underlying REC8's role in neuroblastoma.
- To assess REC8 as a potential therapeutic target for neuroblastoma.
Main Methods:
- Small interfering (si) RNA technology was used to knockdown REC8.
- Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot validated REC8 downregulation.
- Cell Counting Kit-8 (CCK-8), flow cytometry, tube formation assays, and Transwell tests assessed proliferation, cell cycle, apoptosis, angiogenesis, migration, and invasion.
Main Results:
- REC8 downregulation significantly reduced neuroblastoma cell proliferation by inducing G1 phase cell cycle arrest.
- Knockdown of REC8 inhibited cell migration, invasion, and angiogenesis.
- Repressing REC8 expression decreased the activation of the STAT3/VEGF signaling pathway in neuroblastoma cells.
- REC8 knockdown enhanced apoptosis in neuroblastoma cells.
Conclusions:
- Targeting REC8 is a potential therapeutic strategy for neuroblastoma.
- Downregulation of REC8 inhibits key oncogenic processes in neuroblastoma.
- REC8's role in the STAT3/VEGF pathway suggests downstream therapeutic targets.
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