ArticleMolecular biology reports2013
SynCAM, a novel putative tumor suppressor, suppresses growth and invasiveness of glioblastoma.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- SynCAMs in Normal Vertebrate Neural Development and Neuropsychiatric Disorders: from the Perspective of the OCAs.Molecular neurobiology · 2024Review
- Integrating Multi-Omics Analysis for Enhanced Diagnosis and Treatment of Glioblastoma: A Comprehensive Data-Driven Approach.Cancers · 2023Article
- MicroRNA-15a-5p promotes the proliferation and invasion of T98G glioblastoma cells via targeting cell adhesion molecule 1.Oncology letters · 2021Article
- Role of exosomes in malignant glioma: microRNAs and proteins in pathogenesis and diagnosis.Cell communication and signaling : CCS · 2020Review
- Downregulating SynCAM and MPP6 expression is associated with ovarian cancer progression.Oncology letters · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SynCAM, also named by TSLC1, SgIGSF and IGSF4, was identified as a neural tissue-specific immunoglobulin-like cell-cell adhesion molecule. However, the role of SynCAM in tumorigenesis remains elusive. We aimed to clarify its epigenetic regulation and biological functions in glioblastoma. SynCAM was silenced in 72 % (5/7) glioblastoma cell lines. A significant downregulation was also detected in paired glioblastoma tumors compared with adjacent non-cancerous tissues. In contrast, SynCAM was readily expressed in various normal adult brain tissues. Ectopic expression of SynCAM in the silenced cancer cell line T98G significantly reduced colony formation and cell proliferation, induced cell cycle arrests and repressed cell invasive ability. Nude mice were subcutaneously injected into the flank with T98G cells and treated with normal saline, pcDNA3.1 (vector) or pcDNA3.1-SynCAM, respectively. Treatment with pcDNA3.1-SynCAM retarded growth in the xenografts, which contributed to a 58 % decrease in tumor volume compared to controls. In conclusion, our results suggest that SynCAM suppressions growth of glioblastoma and may serve as a novel functional tumor-suppressor gene.
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Registered trials
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