ArticleNeoplasia (New York, N.Y.)2013
Loss of Sh3gl2/endophilin A1 is a common event in urothelial carcinoma that promotes malignant behavior.
Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Integrative Transcriptomic and Interactome Analyses Prioritize Candidate Genes for Alzheimer's Disease.Molecular neurobiology · 2026Article
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- Genome-Wide DNA Methylation Profiling Reveals Ancestry-Associated Epigenetic Reprogramming in Cervical Intraepithelial Neoplasia.International journal of molecular sciences · 2026Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Survival Outcomes in Patients with Squamous Cell Carcinoma of the Urinary Bladder: A Propensity Score-Matched Analysis.Current oncology (Toronto, Ont.) · 2025Observational
- SH3GL2 and MMP17 as lung adenocarcinoma biomarkers: a machine-learning based approach.Biochemistry and biophysics reports · 2024Article
- Biology of endophilin and it's role in disease.Frontiers in immunology · 2023Review
- Bioinformatics Analysis and Experimental Identification of Immune-Related Genes and Immune Cells in the Progression of Retinoblastoma.Investigative ophthalmology & visual science · 2022Article
- Spatial proteomics finds CD155 and Endophilin-A1 as mediators of growth and invasion in medulloblastoma.Life science alliance · 2022Article
- Molecular mechanism of Fast Endophilin-Mediated Endocytosis.The Biochemical journal · 2020Review
- Repression of transcription factor AP-2 alpha by PPARγ reveals a novel transcriptional circuit in basal-squamous bladder cancer.Oncogenesis · 2019Article
- Cancer Testis Antigen Promotes Triple Negative Breast Cancer Metastasis and is Traceable in the Circulating Extracellular Vesicles.Scientific reports · 2019Article
- Quantitative proteomics reveals reduction of endocytic machinery components in gliomas.EBioMedicine · 2019Article
- Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling.Journal of cellular and molecular medicine · 2017Article
- Insights from animal models of bladder cancer: recent advances, challenges, and opportunities.Oncotarget · 2017Review
- Identification of genes and critical control proteins associated with inflammatory breast cancer using network controllability.PloS one · 2017Article
- Distinct Functions of Endophilin Isoforms in Synaptic Vesicle Endocytosis.Neural plasticity · 2015Article
- Aberrant promoter methylation of SH3GL2 gene in vulvar squamous cell carcinoma correlates with clinicopathological characteristics and HPV infection status.International journal of clinical and experimental pathology · 2015Article
- The role of EGFR family inhibitors in muscle invasive bladder cancer: a review of clinical data and molecular evidence.The Journal of urology · 2015Review
- Article
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Urothelial carcinoma (UC) causes substantial morbidity and mortality worldwide. However, the molecular mechanisms underlying urothelial cancer development and tumor progression are still largely unknown. Using informatics analysis, we identified Sh3gl2 (endophilin A1) as a bladder urothelium-enriched transcript. The gene encoding Sh3gl2 is located on chromosome 9p, a region frequently altered in UC. Sh3gl2 is known to regulate endocytosis of receptor tyrosine kinases implicated in oncogenesis, such as the epidermal growth factor receptor (EGFR) and c-Met. However, its role in UC pathogenesis is unknown. Informatics analysis of expression profiles as well as immunohistochemical staining of tissue microarrays revealed Sh3gl2 expression to be decreased in UC specimens compared to nontumor tissues. Loss of Sh3gl2 was associated with increasing tumor grade and with muscle invasion, which is a reliable predictor of metastatic disease and cancer-derived mortality. Sh3gl2 expression was undetectable in 19 of 20 human UC cell lines but preserved in the low-grade cell line RT4. Stable silencing of Sh3gl2 in RT4 cells by RNA interference 1) enhanced proliferation and colony formation in vitro, 2) inhibited EGF-induced EGFR internalization and increased EGFR activation, 3) stimulated phosphorylation of Src family kinases and STAT3, and 4) promoted growth of RT4 xenografts in subrenal capsule tissue recombination experiments. Conversely, forced re-expression of Sh3gl2 in T24 cells and silenced RT4 clones attenuated oncogenic behaviors, including growth and migration. Together, these findings identify loss of Sh3gl2 as a frequent event in UC development that promotes disease progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.