ArticleScientific reports2017
High expression of β-catenin contributes to the crizotinib resistant phenotype in the stem-like cell population in neuroblastoma.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Developmentally relevant proteins contribute to chemotherapeutic resistance in neuroblastoma.Frontiers in oncology · 2026Review
- Bioinformatics analysis of miRNAs in the neuroblastoma 11q-deleted region reveals a role of miR-548l in both 11q-deleted and MYCN amplified tumour cells.Scientific reports · 2022Article
- Correlation of Immunological and Molecular Profiles with Response to Crizotinib in Alveolar Soft Part Sarcoma: An Exploratory Study Related to the EORTC 90101 "CREATE" Trial.International journal of molecular sciences · 2022Article
- Extracellular domain shedding of the ALK receptor mediates neuroblastoma cell migration.Cell reports · 2021Article
- Long Noncoding RNA NHEG1 Drives β-Catenin Transactivation and Neuroblastoma Progression through Interacting with DDX5.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Hypoxia Induces the Acquisition of Cancer Stem-like Phenotype Via Upregulation and Activation of Signal Transducer and Activator of Transcription-3 (STAT3) in MDA-MB-231, a Triple Negative Breast Cancer Cell Line.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018Article
- lincROR influences the stemness and crizotinib resistance in EML-ALKOncoTargets and therapy · 2018Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
ALK has been identified as a novel therapeutic target in neuroblastoma (NB), but resistance to ALK inhibitors (such as crizotinib) is well recognized. We recently published that the crizotinib sensitivity in NB cells strongly correlates with the crizotinib-ALK binding, and β-catenin effectively hinders this interaction and confers crizotinib resistance. Here, we asked if these observations hold true for the stem-like cells in NB cells, which were purified based on their responsiveness to a Sox2 reporter. Compared to bulk, reporter unresponsive (RU) cells, reporter responsive (RR) cells had significantly higher neurosphere formation ability, expression of CD133/nestin and chemo-resistance. Using the cellular thermal shift assay, we found that RR cells exhibited significantly weaker crizotinib-ALK binding and higher crizotinib resistance than RU cells. The suboptimal crizotinib-ALK binding in RR cells can be attributed to their high β-catenin expression, since siRNA knockdown of β-catenin restored the crizotinib-ALK binding and lowered the crizotinib resistance to the level of RU cells. Enforced expression of β-catenin in RU cells resulted in the opposite effects. To conclude, high expression of β-catenin in the stem-like NB cells contributes to their crizotinib resistance. Combining β-catenin inhibitors and ALK inhibitors may be useful in treating NB patients.
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