ArticleOncotarget2017
Protein S drives oral squamous cell carcinoma tumorigenicity through regulation of AXL.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Protein S: a vitamin K-dependent factor bridging haemostasis, tissue homeostasis and cancer.The Biochemical journal · 2026Review
- TAM receptor tyrosine kinases as potential mediators of the non-lytic spread of non-enveloped viruses.Biochemical Society transactions · 2026Review
- TYRO3, AXL, MERTK and Their Ligands in Brain Metastases From Colorectal Cancers.Cancer medicine · 2026Article
- Identification and validation of key biomarkers for chemoresistance in oral squamous cell carcinoma.BMC cancer · 2025Article
- Proteomic Analysis of Serum Samples in Ovulatory Polycystic Ovary Syndrome and Construction of a Protein Interaction Pathway.The protein journal · 2025Article
- Article
- Element-specific estimation of background mutation rates in whole cancer genomes through transfer learning.NPJ precision oncology · 2025Article
- In silico research of coagulation- and fibrinolysis-related genes for predicting prognosis of clear cell renal cell carcinoma.Translational andrology and urology · 2025Article
- Mechanistic insights into PROS1 inhibition of bladder cancer progression and angiogenesis via the AKT/GSK3β/β-catenin pathway.Scientific reports · 2025Article
- The Vitamin K-Dependent Anticoagulant Factor, Protein S, Regulates Vascular Permeability.Current issues in molecular biology · 2024Article
- Article
- AXL, along with PROS1, is overexpressed in papillary thyroid carcinoma and regulates its biological behaviour.World journal of surgical oncology · 2022Article
- New insights into vitamin K biology with relevance to cancer.Trends in molecular medicine · 2022Review
- BAP1 Loss Promotes Suppressive Tumor Immune Microenvironment via Upregulation of PROS1 in Class 2 Uveal Melanomas.Cancers · 2022Article
- LncRNA RP3-525N10.2-NFKB1-PROS1 triplet-mediated low PROS1 expression is an onco-immunological biomarker in low-grade gliomas: a pan-cancer analysis with experimental verification.Journal of translational medicine · 2022Article
- The role of phosphatidylserine on the membrane in immunity and blood coagulation.Biomarker research · 2022Review
- PROS1 shapes the immune-suppressive tumor microenvironment and predicts poor prognosis in glioma.Frontiers in immunology · 2022Article
- Identification and validation of potential novel biomarkers for oral squamous cell carcinoma.Bioengineered · 2021Article
- Phosphatidylserine-Gold Nanoparticles (PS-AuNP) Induce Prostate and Breast Cancer Cell Apoptosis.Pharmaceutics · 2021Article
- Myeloid cell-derived PROS1 inhibits tumor metastasis by regulating inflammatory and immune responses via IL-10.The Journal of clinical investigation · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TAM family of proto-oncogenic receptor protein tyrosine kinases, comprising of TYRO3, AXL, and MERTK, is implicated in many human cancers. Their activation leads to cancer cell proliferation, enhanced migration, invasion, and drug resistance; however how TAMs are activated in cancers is less understood. We previously showed that Protein S (PROS1) is a ligand of the TAM receptors. Here we identify PROS1 as a mediator of Oral Squamous Cell Carcinoma (OSCC) in proliferation, cell survival and migration. We demonstrate that excess PROS1 induces OSCC proliferation and migration. Conversely, blocking endogenous PROS1 expression using shRNA significantly inhibits cell proliferation and migration in culture. This inhibition was rescued by the addition of purified PROS1. Moreover, PROS1 knockdown reduced anchorage-independent growth in-vitro, reduced tumor xenograft growth in nude mice and altered their differentiation profile. Mechanistically, we identify the downregulation of AXL transcripts and protein following PROS1 knockdown. Re-introducing PROS1 rescues AXL expression both at the protein and transcriptional levels. The anti-proliferative effect of the AXL inhibitor R428 was significantly reduced following PROS1 inhibition, indicating the functional significance of PROS1-mediated regulation of AXL in OSCC. Taken together, we identify PROS1 as a driver of OSCC tumor growth and a modulator of AXL expression. Our results point to PROS1 as a potential novel anti-cancer therapeutic target.
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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.