ArticleJournal of molecular medicine (Berlin, Germany)2013
SH3GL2 is frequently deleted in non-small cell lung cancer and downregulates tumor growth by modulating EGFR signaling.
Article in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
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- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- A network-based analysis to identify a piRNA-target signature related to colorectal cancer prognosis: in silico and in vitro study.Discover oncology · 2025Article
- SH3GL2 and MMP17 as lung adenocarcinoma biomarkers: a machine-learning based approach.Biochemistry and biophysics reports · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Identification of Hub Genes in Pediatric Medulloblastoma by Multiple-Microarray Analysis.Journal of molecular neuroscience : MN · 2020Article
- Identification of differentially expressed genes between primary lung cancer and lymph node metastasis via bioinformatic analysis.Oncology letters · 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
- Decreased expression of USP9X is associated with poor prognosis in Chinese pancreatic ductal adenocarcinoma patients.Oncology letters · 2018Article
- 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
- Identification of genes and critical control proteins associated with inflammatory breast cancer using network controllability.PloS one · 2017Article
- Integrated Analysis of DNA Methylation and mRNA Expression Profiles Data to Identify Key Genes in Lung Adenocarcinoma.BioMed research international · 2016Article
- Uncovering Driver DNA Methylation Events in Nonsmoking Early Stage Lung Adenocarcinoma.BioMed research international · 2016Article
- Targeting HER (ERBB) signaling in head and neck cancer: An essential update.Molecular aspects of medicine · 2015Review
- Context-dependent function of the deubiquitinating enzyme USP9X in pancreatic ductal adenocarcinoma.Cancer biology & therapy · 2014Article
- Article
- Loss of Sh3gl2/endophilin A1 is a common event in urothelial carcinoma that promotes malignant behavior.Neoplasia (New York, N.Y.) · 2013Article
- Overexpression of EGFR in head and neck squamous cell carcinoma is associated with inactivation of SH3GL2 and CDC25A genes.PloS one · 2013Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
The purpose of this study was to identify key genetic pathways involved in non-small cell lung cancer (NSCLC) and understand their role in tumor progression. We performed a genome wide scanning using paired tumors and corresponding 16 mucosal biopsies from four follow-up lung cancer patients on Affymetrix 250K-NSpI array platform. We found that a single gene SH3GL2 located on human chromosome 9p22 was most frequently deleted in all the tumors and corresponding mucosal biopsies. We further validated the alteration pattern of SH3GL2 in a substantial number of primary NSCLC tumors at DNA and protein level. We also overexpressed wild-type SH3GL2 in three NSCLC cell lines to understand its role in NSCLC progression. Validation in 116 primary NSCLC tumors confirmed frequent loss of heterozygosity of SH3GL2 in overall 51 % (49/97) of the informative cases. We found significantly low (p = 0.0015) SH3GL2 protein expression in 71 % (43/60) primary tumors. Forced overexpression of wild-type (wt) SH3GL2 in three NSCLC cell lines resulted in a marked reduction of active epidermal growth factor receptor (EGFR) expression and an increase in EGFR internalization and degradation. Significantly decreased in vitro (p = 0.0015-0.030) and in vivo (p = 0.016) cellular growth, invasion (p = 0.029-0.049), and colony formation (p = 0.023-0.039) were also evident in the wt-SH3GL2-transfected cells accompanied by markedly low expression of activated AKT(Ser(473)), STAT3 (Tyr(705)), and PI3K. Downregulation of SH3GL2 interactor USP9X and activated ß-catenin was also evident in the SH3GL2-transfected cells. Our results indicate that SH3GL2 is frequently deleted in NSCLC and regulates cellular growth and invasion by modulating EGFR function.
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