ArticleCell death discovery2022
FAS receptor regulates NOTCH activity through ERK-JAG1 axis activation and controls oral cancer stemness ability and pulmonary metastasis.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- PCYT2 inhibits lipid accumulation via the notch signaling pathway in chicken primary hepatocytes.Poultry science · 2026Article
- Inhibition of the EP300/Notch Signaling Pathway Regulates Proliferation and Apoptosis in Oral Squamous Cell Carcinoma.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Article
- Targeting the Notch signaling pathway in digestive system cancers: from bench to bedside.Cancer cell international · 2026Review
- CAVIN3 deficiency promotes vascular normalization in ocular neovascular disease via ERK/JAG1 signaling pathway.JCI insight · 2025Article
- The miR-876-5p/SOCS4/STAT3 pathway induced the expression of PD-L1 and suppressed antitumor immune responses.Cancer cell international · 2025Article
- Oral Cancer-Derived miR-762 Suppresses T-Cell Infiltration and Activation by Horizontal Inhibition of CXCR3 Expression.International journal of molecular sciences · 2025Article
- JAG1/Notch Pathway Inhibition Induces Ferroptosis and Promotes Cataractogenesis.International journal of molecular sciences · 2025Article
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- MEK/ERK signaling drives the transdifferentiation of supporting cells into functional hair cells by modulating the Notch pathway.Stem cells translational medicine · 2024Article
- Sacubitril/valsartan inhibits the proliferation of vascular smooth muscle cells through notch signaling and ERK1/2 pathway.BMC cardiovascular disorders · 2024Article
- FAS gene expression, prognostic significance and molecular interactions in lung cancer.Frontiers in oncology · 2024Article
- Revealing spatial multimodal heterogeneity in tissues with SpaTrio.Cell genomics · 2023Article
- High expression of HSP60 and survivin predicts poor prognosis for oral squamous cell carcinoma patients.BMC oral health · 2023Article
- Targeted inhibition of eIF5ACell death & disease · 2023Article
- Panoramic view of key cross-talks underpinning the oral squamous cell carcinoma stemness - unearthing the future opportunities.Frontiers in oncology · 2023Review
- The role of Hedgehog and Notch signaling pathway in cancer.Molecular biomedicine · 2022Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Pulmonary metastasis occurring via the colonization of circulating cancer stem cells is a major cause of oral squamous cell carcinoma (OSCC)-related death. Thus, understanding the mechanism of OSCC pulmonary metastasis may provide a new opportunity for OSCC treatment. FAS, a well-known apoptosis-inducing death receptor, has multiple nonapoptotic, protumorigenic functions. Previously, we found that SAS OSCC cells with FAS receptor knockout did not affect orthotopic tumor growth or cervical lymph node metastasis. However, FAS knockout cells could not colonize in distant organs to form metastases upon intravenous injection, which hinted at the cancer stemness function of the FAS receptor. Immunohistochemistry staining indicated that the FAS receptor serves as a poor prognosis marker in OSCC patients. FAS knockout inhibited in vitro cancer spheroid formation, migration and invasion, and prevented mesenchymal transition in OSCC cells and inhibited OSCC pulmonary metastasis in vivo. To determine the regulatory mechanism by which the FAS receptor exerts its oncogenic function, we utilized cDNA microarrays and phosphoprotein arrays to discover key candidate genes and signaling pathway regulators. JAG1 expression and NOTCH pathway activation were controlled by the FAS receptor through ERK phosphorylation. Both JAG1 and NOTCH1 silencing decreased in vitro cancer spheroid formation. In OSCC cells, FAS ligand or JAG1 protein treatment increased NOTCH pathway activity, which could be abolished by FAS receptor knockout. In FAS knockout cells, restoring the NOTCH1 intracellular domain stimulated cancer spheroid formation. Both JAG1 and NOTCH1 silencing decreased in vivo OSCC growth. In conclusion, we found a novel FAS-ERK-JAG1-NOTCH1 axis that may contribute to OSCC stemness and pulmonary metastasis.
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Registered trials
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.