ArticleMolecular carcinogenesis2014
Up-regulated cten by FGF2 contributes to FGF2-mediated cell migration.
Article in Molecular carcinogenesis, 2014. 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, 30 citations in OpenAlex.
- FGF2 as a Potential Tumor Suppressor in Lung Adenocarcinoma.Diagnostics (Basel, Switzerland) · 2026Article
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- miR-16a-5p antagonizes FGF-2 in ligamentogenic differentiation of MSC: a new therapeutic perspective for tendon regeneration.Scientific reports · 2024Article
- The role of tensins in malignant neoplasms.Archives of medical science : AMS · 2023Article
- Increased tensin 4 expression is related to the histological type of gastric cancer.World journal of clinical oncology · 2021Article
- CTEN Induces Tumour Cell Invasion and Survival and Is Prognostic in Radiotherapy-Treated Head and Neck Cancer.Cancers · 2020Article
- Semen Modulates the Expression of NGF, ABHD2, VCAN, and CTEN in the Reproductive Tract of Female Rabbits.Genes · 2020Article
- Tensin4 (TNS4) is upregulated by Wnt signalling in adenomas in multiple intestinal neoplasia (Min) mice.International journal of experimental pathology · 2020Article
- Article
- Identification of subcellular targeting sequences of Cten reveals its role in cell proliferation.Biochimica et biophysica acta. Molecular cell research · 2019Article
- TGFβ1-induced cell motility but not cell proliferation is mediated through Cten in colorectal cancer.International journal of experimental pathology · 2018Article
- Overexpression of CTEN relates to tumor malignant potential and poor outcomes of adenocarcinoma of the esophagogastric junction.Oncotarget · 2017Article
- Multiple pathways regulate Cten in colorectal cancer without a Tensin switch.International journal of experimental pathology · 2015Article
- The impact of RNA binding motif protein 4-regulated splicing cascade on the progression and metabolism of colorectal cancer cells.Oncotarget · 2015Article
- Tensin4 is up-regulated by EGF-induced ERK1/2 activity and promotes cell proliferation and migration in hepatocellular carcinoma.Oncotarget · 2015Article
- Il-6 signaling between ductal carcinoma in situ cells and carcinoma-associated fibroblasts mediates tumor cell growth and migration.BMC cancer · 2015Article
- C-terminal tensin-like protein mediates invasion of human lung cancer cells and is regulated by signal transducer and activator of transcription 3.The Journal of thoracic and cardiovascular surgery · 2015Article
- C-terminal tensin-like (CTEN): a promising biomarker and target for cancer.The international journal of biochemistry & cell biology · 2014Review
- CTEN prolongs signaling by EGFR through reducing its ligand-induced degradation.Cancer research · 2013Article
- C-terminal tensin-like protein is a novel prognostic marker for primary melanoma patients.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cten is a focal adhesion molecule that is expressed at very low levels in most normal tissues. Nonetheless, its expression has been found to increase dramatically in many types of cancer including colorectal, breast, gastric, and pancreatic cancer, suggesting that cten may play a critical role during tumorigenesis. To study the mechanisms that induce cten expression and the function of up-regulated cten, we examined the effects of several cancer-associated growth factors and cytokines on cten expression. We found that EGF, FGF2, NGF, PDGF, TGF-β, IGF-1, IL-6, and IL-13 were able to induce cten expression in a dose- and time-dependent manner. The Mek-Erk and PI3K-Akt pathways were two main signaling cascades responsible for cten up-regulation, whereas the Jak-Stat pathway could contribute to the increase in some conditions. Since many of these factors are known to promote cell migration, we hypothesized that up-regulated cten might contribute to this process. This hypothesis was investigated in FGF2-mediated cell migration. Silencing of cten not only reduced regular cell motility but also FGF2-mediated cell migration. Overexpression of cten promoted cell migration and FGF2 treatment failed to further enhance cell migration. Our findings that (1) cten is a common downstream molecule of these cancer-associated growth factors and cytokines; and that (2) up-regulated cten modulates cell migration induced by FGF2 and likely other growth factors as well, strongly suggest that cten could be a potential downstream therapeutic target for treating cancers associated with aberrant signaling of these growth factors and cytokines.
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