ArticleExperimental & molecular medicine2014
Syntenin increases the invasiveness of small cell lung cancer cells by activating p38, AKT, focal adhesion kinase and SP1.
Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Phosphorylation of syntenin-1 by TBK1 promotes proliferation and migration of non-small cell lung cancer cells.The Journal of biological chemistry · 2025Article
- Current and future therapies for small cell lung carcinoma.Journal of hematology & oncology · 2025Review
- The Multifunctional Protein Syntenin-1: Regulator of Exosome Biogenesis, Cellular Function, and Tumor Progression.International journal of molecular sciences · 2023Review
- Biological Role and Aberrant Overexpression of Syntenin-1 in Cancer: Potential Role as a Biomarker and Therapeutic Target.Biomedicines · 2023Review
- Inhibitors against Two PDZ Domains of MDA-9 Suppressed Migration of Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Huaier Inhibits Gastric Cancer Growth and Hepatic Metastasis by Reducing Syntenin Expression and STAT3 Phosphorylation.Journal of oncology · 2022Article
- Article
- Syntenin overexpression in human lung cancer tissue and serum is associated with poor prognosis.BMC cancer · 2020Article
- Nutraceutical Compounds as Sensitizers for Cancer Treatment in Radiation Therapy.International journal of molecular sciences · 2019Review
- Syntenin: PDZ Protein Regulating Signaling Pathways and Cellular Functions.International journal of molecular sciences · 2019Review
- A PDZ Protein MDA-9/Syntenin: As a Target for Cancer Therapy.Computational and structural biotechnology journal · 2019Review
- Hsa-miR-370 inhibited P-selectin-induced cell adhesion in human colon adenocarcinoma cells.Molecular and cellular biochemistry · 2019Article
- Article
- MDA-9/Syntenin-Slug transcriptional complex promote epithelial-mesenchymal transition and invasion/metastasis in lung adenocarcinoma.Oncotarget · 2016Article
- High expression of AKR1C1 is associated with proliferation and migration of small-cell lung cancer cells.Lung Cancer (Auckland, N.Z.) · 2016Article
- The Genetic Architecture of Murine Glutathione Transferases.PloS one · 2016Article
- Examination of Epigenetic and other Molecular Factors Associated with mda-9/Syntenin Dysregulation in Cancer Through Integrated Analyses of Public Genomic Datasets.Advances in cancer research · 2015Review
- Targeting tumor invasion: the roles of MDA-9/Syntenin.Expert opinion on therapeutic targets · 2015Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Syntenin is a PDZ domain-containing adaptor protein that has been recently shown to regulate migration and invasion in several tumors. Small cell lung cancer (SCLC) is notorious for its invasiveness and strong potential for metastasis. We therefore studied the influence of syntenin on the invasiveness of SCLC. Immunohistochemistry in tumor tissues showed that syntenin was more frequently expressed in small cell carcinomas than other neuroendocrine tumors, such as carcinoids and neuroblastomas, suggesting that syntenin expression may be related to more aggressive forms of neuroendocrine tumors. In SCLC patients, syntenin overexpression in tumor cells was significantly associated with more extensive and advanced disease at the time of diagnosis (P=0.029). Overexpression of syntenin in SCLC cells that were intrinsically syntenin-low increased the invasiveness of cells and led to the induction of extracellular matrix (ECM)-degrading membrane type 1-matrix metalloproteinase (MT1-MMP) and matrix metalloproteinase 2 (MMP2). In contrast, suppression of syntenin in syntenin-high cells was associated with the downregulation of MT1-MMP. Contrary to the results of previous studies using malignant melanomas and breast carcinomas, signaling cascades were shown to be further transduced through p38 MAPK and PI3K/AKT, with activation of SP1 rather than NF-κB, under circumstances not involving ECM interaction. In addition, the upstream molecule focal adhesion kinase was induced by syntenin activation, in spite of the absence of ECM interaction. These results suggest that syntenin might contribute to the invasiveness of SCLC and could be utilized as a new therapeutic target for controlling invasion and metastasis in SCLC.
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