ArticlePloS one2017
ALK signaling cascade confers multiple advantages to glioblastoma cells through neovascularization and cell proliferation.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Hypoxia-inducible factor 1alpha and vascular endothelial growth factor in Glioblastoma Multiforme: a systematic review going beyond pathologic implications.Oncology research · 2024Pooled it
- Precision oncology in a dish: patient-derived glioma organoids to guide novel therapeutic strategies.Biomarker research · 2026Article
- Multi-Omics and Single-Cell Dissection of Exostosin Glycosyltransferases (EXT1/EXT2) Reveals Divergent Oncogenic Roles and Therapeutic Vulnerabilities in Gliomas.Journal of Cancer · 2026Article
- The Roles of RNA-Binding Proteins in Vasculogenic Mimicry Regulation in Glioblastoma.International journal of molecular sciences · 2025Review
- SOX4-BMI1 axis promotes non-small cell lung cancer progression and facilitates angiogenesis by suppressing ZNF24.Cell death & disease · 2024Article
- Evaluation of Immunohistochemical Expression of ALK-1 in Gliomas, WHO Grade 4 and Its Correlation with IDH1-R132H Mutation Status.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Anaplastic lymphoma kinase overexpression enhances aggressive phenotypic characteristics of endometrial carcinoma.BMC cancer · 2023Article
- Temozolomide protects against the progression of glioblastoma via SOX4 downregulation by inhibiting the LINC00470-mediated transcription factor EGR2.CNS neuroscience & therapeutics · 2023Article
- Article
- A functional role of S100A4/non-muscle myosin IIA axis for pro-tumorigenic vascular functions in glioblastoma.Cell communication and signaling : CCS · 2022Article
- Prognostic role of ALK-1 and h-TERT expression in glioblastoma multiforme: correlation with ALK gene alterations.Journal of pathology and translational medicine · 2021Article
- Prognostic and predictive markers in glioblastoma and ALK overexpression.Journal of pathology and translational medicine · 2021Article
- The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.Frontiers in oncology · 2021Article
- Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies.International journal of molecular sciences · 2020Review
- Phosphorylated STAT3 expression linked toOncology letters · 2020Article
- ALK Inhibitors-Induced M Phase Delay Contributes to the Suppression of Cell Proliferation.Cancers · 2020Article
- cMyc and ERK activity are associated with resistance to ALK inhibitory treatment in glioblastoma.Journal of neuro-oncology · 2020Article
- Targeting Autophagy in ALK-Associated Cancers.Cancers · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic lymphoma kinase (ALK), which is a receptor tyrosine kinase, is essentially and transiently expressed in the developing nervous system. Here we examined the functional role of the ALK gene in glioblastomas (GBMs). In clinical samples of GBMs, high ALK expression without gene rearrangements or mutations was frequently observed in perivascular lesions, in contrast to the relatively low expression in the perinecrotic areas, which was positively correlated with N-myc and phosphorylated (p) Stat3 scores and Ki-67 labeling indices. ALK immunoreactivity was also found to be associated with neovascular features including vascular co-option and vascular mimicry. In astrocytoma cell lines, cells stably overexpressing full-length ALK showed an increase in expression of pStat3 and pAkt proteins, as well as hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor-A (VEGF-A) mRNAs, in contrast to cells with knockdown of endogenous ALK which showed decreased expression of these molecules. Transfection of the constitutively active form of Stat3 induced an increase in HIF-1α promoter activity, and the overexpression of HIF-1α in turn resulted in enhancement of VEGF-A promoter activity. In addition, cells with overexpression or knockdown of ALK also showed a tendency toward increased and decreased proliferation, respectively, through changes in expression of pAkt and pStat3. Finally, ALK promoter was significantly activated by transfection of Sox4 and N-myc, which are known to contribute to neuronal properties. These findings therefore suggest that N-myc/Sox4-mediated ALK signaling cascades containing Stat3, Akt, HIF-1α, and VEGF-A confer multiple advantages to tumor growth through alterations in neovascularization and cell proliferation in GBMs.
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