ArticleBMC cancer2019
The small molecule Bcl-2/Mcl-1 inhibitor TW-37 shows single-agent cytotoxicity in neuroblastoma cell lines.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Pharmacologic inhibition of BMI1 exerts antitumor effects against MYCN-amplified neuroblastoma, with activation of the p53 pathway.Scientific reports · 2025Article
- Single-cell technology reveals the crosstalk between tumor cells and immune cells: driving immune signal transduction and inflammation-mediated cardiac dysfunction in the tumor microenvironment of colorectal cancer.Frontiers in immunology · 2025Article
- Targeting the apoptosis pathway to treat tumours of the paediatric nervous system.Cell death & disease · 2022Review
- Acute toxicity analysis of an inhibitor of BCL2, Disarib, in rats.Scientific reports · 2021Article
- Synergistic Effects of TW-37 and ABT-263 on Renal Cell Carcinoma Cells.Cancer management and research · 2021Article
- Gastric cancer: a comprehensive review of current and future treatment strategies.Cancer metastasis reviews · 2020Review
- The Anti-Apoptotic Role of EBV-LMP1 in Lymphoma Cells.Cancer management and research · 2020Article
- Cryptotanshinone chemosensitivity potentiation by TW-37 in human oral cancer cell lines by targeting STAT3-Mcl-1 signaling.Cancer cell international · 2020Article
- Vitamin K3 derivative induces apoptotic cell death in neuroblastoma via downregulation of MYCN expression.Biochemistry and biophysics reports · 2019Article
- Destined to Die: Apoptosis and Pediatric Cancers.Cancers · 2019Review
- Antitumor effect of TW-37, a BH3 mimetic in human oral cancer.Laboratory animal research · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh-risk neuroblastoma with N-Myc amplification remains a therapeutic challenge in paediatric oncology. Antagonism of pro-death Bcl-2 homology (BH) proteins to pro-survival BH members such as Mcl-1 and Bcl-2 has become a treatment approach, but previous studies suggest that a combined inhibition of Bcl-2 and Mcl-1 is necessary. TW-37 inhibits Mcl-1 and Bcl-2 with almost the same affinity. However, single-agent cytotoxicity of TW-37 in neuroblastoma cell lines has not been investigated.
methodsCell viability, apoptosis, proliferation and changes in growth properties were determined in SKNAS, IMR-5, SY5Y and Kelly cells after treatment with TW-37. After transfection with Mcl-1 or Bcl-2 siRNA, apoptosis and proliferation were investigated in Kelly cells. Mice with Kelly cell line xenografts were treated with TW-37 and tumor growth, survival and apoptosis were determined.
resultsCell lines with N-Myc amplification were more sensitive to TW-37 treatment, IC50 values for IMR-5 and Kelly cells being 0.28 μM and 0.22 μM, compared to SY5Y cells and SKNAS cells (IC50 0.96 μM and 0.83 μM). Treatment with TW-37 resulted in increased apoptosis and reduced proliferation rates, especially in IMR5 and Kelly cells. Bcl-2 as well as Mcl-1 knockdown induced apoptosis in Kelly cells. TW-37 led to a decrease in tumor growth and a favorable survival (p = 0.0379) in a Kelly neuroblastoma xenografts mouse model.
conclusionTW-37 has strong single-agent cytotoxicity in vitro and in vivo. Therefore, combined inhibition of Bcl-2/Mcl-1 by TW-37 in N-Myc amplified neuroblastoma may represent an interesting therapeutic strategy.
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