ArticleOncogene2013
Fas signaling promotes motility and metastasis through epithelial-mesenchymal transition in gastrointestinal cancer.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer.Cells, tissues, organs · 2021Pooled it
- Review
- Tumor necrosis factor superfamily signaling: life and death in cancer.Cancer metastasis reviews · 2024Review
- Microarray-based detection and expression analysis of drug resistance in an animal model of peritoneal metastasis from colon cancer.Clinical & experimental metastasis · 2024Article
- Article
- Role of non-coding RNAs as new therapeutic targets in regulating the EMT and apoptosis in metastatic gastric and colorectal cancers.Cell cycle (Georgetown, Tex.) · 2023Review
- Evaluation of ITGB1 expression as a predictor of the therapeutic effects of immune checkpoint inhibitors in gastric cancer.BMC gastroenterology · 2023Article
- The SKA3-DUSP2 Axis Promotes Gastric Cancer Tumorigenesis and Epithelial-Mesenchymal Transition by Activating the MAPK/ERK Pathway.Frontiers in pharmacology · 2022Article
- Epithelial-mesenchymal transition-related long noncoding RNAs in gastric carcinoma.Frontiers in molecular biosciences · 2022Review
- CD95/Fas protects triple negative breast cancer from anti-tumor activity of NK cells.iScience · 2021Article
- Epithelial-specific ERBB3 deletion results in a genetic background-dependent increase in intestinal and colon polyps that is mediated by EGFR.PLoS genetics · 2021Article
- Significance of tumor mutation burden and immune infiltration in thymic epithelial tumors.Thoracic cancer · 2021Article
- SOX2 promotes chemoresistance, cancer stem cells properties, and epithelial-mesenchymal transition by β-catenin and Beclin1/autophagy signaling in colorectal cancer.Cell death & disease · 2021Article
- High FAS expression correlates with a better prognosis and efficacy of taxanes and target regents in breast cancer.Cancer biomarkers : section A of Disease markers · 2021Article
- Transcriptional analysis of cleft palate in TGFβ3 mutant mice.Scientific reports · 2020Article
- Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma.Cancers · 2020Review
- The Role of Circulating Tumor Cells in the Metastatic Cascade: Biology, Technical Challenges, and Clinical Relevance.Cancers · 2020Review
- In silico analysis of the prognostic value of FAS mRNA in malignancies.Journal of Cancer · 2020Article
- ATXN2L upregulated by epidermal growth factor promotes gastric cancer cell invasiveness and oxaliplatin resistance.Cell death & disease · 2019Article
- Caspase-independent cell death does not elicit a proliferative response in melanoma cancer cells.BMC cell biology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas signaling was reported to participate in cell apoptosis. However, this pathway has also been shown to promote tumor cell motility, leading to the hypothesis that Fas signaling may induce epithelial-mesenchymal transition (EMT) to promote metastasis. The effects of Fas-ligand (FasL) treatment and inhibition of Fas signaling on colorectal and gastric cancer cells were tested using motility assay, immunofluorescence, RT-PCR and immunoblot analyses. Fas signaling downregulated epithelial markers, upregulated mesenchymal markers and promoted motility in gastrointestinal (GI) cancer cells. FasL treatment also increased the expression of EMT transcriptional factors in the nucleus and induced a spindle shape cell morphology in these cells. Knockdown of Snail or Twist expression significantly decreased FasL-induced motility. The ERK1/2 pathway was activated by Fas signaling and is required for FasL-induced EMT and motility. Moreover, oxaliplatin, a chemotherapeutic agent, induced EMT partly through Fas signaling. Evaluation of human GI clinical specimens showed that FasL expression increased whereas E-cadherin expression decreased during GI cancer progression. Both markers were significantly inversely correlated. Tissue samples with a non-EMT phenotype were mainly distributed in patients with early cancer stages, whereas samples with an EMT phenotype were mostly distributed in patients with advanced cancer stages. A non-EMT phenotype significantly correlated with better prognosis. Altogether, these data indicate that Fas signaling may induce EMT to promote tumor motility and metastasis in GI cancer in vivo and in vitro.
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