ArticleOncogenesis2020
DDIAS promotes STAT3 activation by preventing STAT3 recruitment to PTPRM in lung cancer cells.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- LAMB1 accelerates esophageal squamous cell carcinoma by triggering JAK2/STAT3 signaling.Molecular biology reports · 2026Article
- Comprehensive characterization of non-small cell lung cancer of different PD-L1 expression classes: a study of 1,038 Chinese patients.Journal of thoracic disease · 2026Article
- Pan-cancer analysis reveals DDIAS as a potential diagnostic biomarker, prognostic indicator, and tumor-immune correlate.Discover oncology · 2026Article
- Bibliometrics and potential gene analysis of post-translational modifications in lung cancer.Journal of thoracic disease · 2025Article
- Dissecting crosstalk induced by cell-cell communication using single-cell transcriptomic data.Nature communications · 2025Article
- Novel carbazole attenuates vascular remodeling through STAT3/CIAPIN1 signaling in vascular smooth muscle cells.Acta pharmaceutica Sinica. B · 2025Article
- Article
- DNA Damage-Induced Apoptosis Suppressor Triggers Progression and Stemness of Glioma by Enhancing Lymphoid Enhancer-Binding Factor 1 Expression.World journal of oncology · 2024Article
- Cellular and clinical impact of protein phosphatase enzyme epigenetic silencing in multiple cancer tissues.Human genomics · 2024Article
- Protein tyrosine phosphatase PTPRO represses lung adenocarcinoma progression by inducing mitochondria-dependent apoptosis and restraining tumor metastasis.Cell death & disease · 2024Article
- Monozygotic triplets with juvenile-onset autoimmunity and 18p microdeletion involvingFrontiers in genetics · 2024Article
- Role of protein tyrosine phosphatase receptor type M in epithelial ovarian cancer progression.Journal of ovarian research · 2023Article
- DDIAS, DNA damage-induced apoptosis suppressor, is a potential therapeutic target in cancer.Experimental & molecular medicine · 2023Review
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- Article
- PSPC1 is a potential prognostic marker for hormone-dependent breast cancer patients and modulates RNA processing of ESR1 and SCFD2.Scientific reports · 2022Article
- Decursin inhibits tumor progression in head and neck squamous cell carcinoma by downregulating CXCR7 expressionOncology reports · 2022Article
- Construction of the miRNA-mRNA Regulatory Networks and Explore Their Role in the Development of Lung Squamous Cell Carcinoma.Frontiers in molecular biosciences · 2022Article
- Role of STAT3 in the pathogenesis of nasopharyngeal carcinoma and its significance in anticancer therapy.Frontiers in oncology · 2022Review
- PTPRM Is Critical for Synapse Formation Regulated by Zinc Ion.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
DNA damage-induced apoptosis suppressor (DDIAS) regulates cancer cell survival. Here we investigated the involvement of DDIAS in IL-6-mediated signaling to understand the mechanism underlying the role of DDIAS in lung cancer malignancy. We showed that DDIAS promotes tyrosine phosphorylation of signal transducer and activator of transcription 3 (STAT3), which is constitutively activated in malignant cancers. Interestingly, siRNA protein tyrosine phosphatase (PTP) library screening revealed protein tyrosine phosphatase receptor mu (PTPRM) as a novel STAT3 PTP. PTPRM knockdown rescued the DDIAS-knockdown-mediated decrease in STAT3 Y705 phosphorylation in the presence of IL-6. However, PTPRM overexpression decreased STAT3 Y705 phosphorylation. Moreover, endogenous PTPRM interacted with endogenous STAT3 for dephosphorylation at Y705 following IL-6 treatment. As expected, PTPRM bound to wild-type STAT3 but not the STAT3 Y705F mutant. PTPRM dephosphorylated STAT3 in the absence of DDIAS, suggesting that DDIAS hampers PTPRM/STAT3 interaction. In fact, DDIAS bound to the STAT3 transactivation domain (TAD), which competes with PTPRM to recruit STAT3 for dephosphorylation. Thus we show that DDIAS prevents PTPRM/STAT3 binding and blocks STAT3 Y705 dephosphorylation, thereby sustaining STAT3 activation in lung cancer. DDIAS expression strongly correlates with STAT3 phosphorylation in human lung cancer cell lines and tissues. Thus DDIAS may be considered as a potential biomarker and therapeutic target in malignant lung cancer cells with aberrant STAT3 activation.
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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.