ArticlePloS one2015
Loss-of-Function PTPRD Mutations Lead to Increased STAT3 Activation and Sensitivity to STAT3 Inhibition in Head and Neck Cancer.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 65 citations in OpenAlex.
- Prospective tumour mutation burden and neoantigen profiling predicts immunotherapy response in metastatic melanoma.NPJ precision oncology · 2026Article
- Synaptic and Non-Synaptic Functions of PTPRD: A Receptor Tyrosine Phosphatase at the Crossroads of Neural Circuitry and Metabolism.Journal of neurochemistry · 2025Review
- p53-regulated SESN1 and SESN2 regulate cell proliferation and cell death through control of STAT3.Cell communication and signaling : CCS · 2025Article
- Neural conditional ablation of the protein tyrosine phosphatase receptor Delta PTPRD impairs gliogenesis in the developing mouse brain cortex.Frontiers in cell and developmental biology · 2024Article
- Robust small molecule-aided cardiac reprogramming systems selective to cardiac fibroblasts.iScience · 2023Article
- Identification of single nucleotide polymorphisms (SNPs) associated with chronic graft-versus-host disease in patients undergoing allogeneic hematopoietic cell transplantation.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2023Article
- Article
- Mutual connected IL-6, EGFR and LIN28/Let7-related mechanisms modulate PD-L1 and IGF upregulation in HNSCC using immunotherapy.Frontiers in oncology · 2023Review
- Electroporation in Head-and-Neck Cancer: An Innovative Approach with Immunotherapy and Nanotechnology Combination.Cancers · 2022Review
- Discovery of Novel Small-Molecule Scaffolds for the Inhibition and Activation of WIP1 Phosphatase from a RapidFire Mass Spectrometry High-Throughput Screen.ACS pharmacology & translational science · 2022Article
- Review
- PTPRD and CNTNAP2 as markers of tumor aggressiveness in oligodendrogliomas.Scientific reports · 2022Article
- Protein tyrosine phosphatase receptor δ serves as the orexigenic asprosin receptor.Cell metabolism · 2022Article
- Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma.Blood · 2022Article
- Whole genome analysis reveals the genomic complexity in metastatic cutaneous squamous cell carcinoma.Frontiers in oncology · 2022Article
- JAK/STAT of all trades: linking inflammation with cancer development, tumor progression and therapy resistance.Carcinogenesis · 2021Article
- Tumor-derived exosomal miR-19b-3p facilitates M2 macrophage polarization and exosomal LINC00273 secretion to promote lung adenocarcinoma metastasis via Hippo pathway.Clinical and translational medicine · 2021Article
- Targeting STAT3 Signaling Pathway in Colorectal Cancer.Biomedicines · 2021Review
- Profile of Basal Cell Carcinoma Mutations and Copy Number Alterations - Focus on Gene-Associated Noncoding Variants.Frontiers in oncology · 2021Article
- Tumor NLRP3-Derived IL-1β Drives the IL-6/STAT3 Axis Resulting in Sustained MDSC-Mediated Immunosuppression.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundProtein tyrosine phosphatase receptor type D (PTPRD) is a putative tumor suppressor in several cancers including head and neck squamous cell carcinoma (HNSCC). STAT3 is a frequently hyperactivated oncogene in HNSCC. As STAT3 is a direct substrate of PTPRD, we sought to determine the genetic or epigenetic alterations of PTPRD that contribute to overactive STAT3 in HNSCC.
methodsWe analyzed data from The Cancer Genome Atlas (TCGA) and our previous whole-exome sequencing study and summarized the mutation, methylation, and copy number status of PTPRD in HNSCC and other cancers. In vitro studies involved standard transfection and MTT protocols, as well as methylation-specific PCR.
resultsOur findings indicate that PTPRD mutation, rather than methylation or copy number alteration, is the primary mechanism by which PTPRD function is lost in HNSCC. We demonstrate that overexpression of wild-type PTPRD in HNSCC cells significantly inhibits growth and STAT3 activation while PTPRD mutants do not, suggesting that mutation may lead to loss of function and subsequent hyper-phosphorylation of PTPRD substrates, especially STAT3. Importantly, we determined that HNSCC cells harboring an endogenous PTPRD mutation are more sensitive to STAT3 blockade than PTPRD wild-type cells. We additionally found that PTPRD mRNA expression does not correlate with pSTAT3 expression, suggesting that alterations that manifest through altered mRNA expression, including hypermethylation and gene copy number alterations, do not significantly contribute to STAT3 overactivation in HNSCC.
conclusionPTPRD mutation, but not methylation or copy number loss, may serve as a predictive biomarker of sensitivity to STAT3 inhibitors in HNSCC.
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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.