ArticleiScience2025
Uncovering the individual immunotherapeutic roles of PTPN1 and PTPN2 in T cells during dual inhibition.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Uncompetitive Allosteric Inhibition of PTP1B by BP-1-102 Reveals a Potential Dual-Target Strategy toward the PTP1B-STAT3 Oncogenic Axis: Biochemical and Computational Evidence.ACS medicinal chemistry letters · 2026Article
- PTPN1/PTPN2 inhibition improves NK cancer therapy by enhancing IL-2 and mitigating TGFβ1 responses.EMBO reports · 2026Article
- Phosphatases in tumor cell immune escape: a perspective based on the camouflage, coercion, cytoprotection.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer immunotherapy benefits only a subset of tumor types, underscoring the need for new targets. The protein tyrosine phosphatases PTPN1 and PTPN2 have emerged as promising candidates and stand out for being amenable to small-molecule inhibition. However, competitive inhibitors inhibit both phosphatases equally, leaving a gap in our understanding of their individual contributions. Herein, we dissected the impact of single and double PTPN1/2 deletion on T cell cytotoxicity. Our results show that while PTPN2 functionally dominates over PTPN1, additional deletion of PTPN1 is required for maximal effect. Transcriptomic profiling revealed that dual deficiency synergistically enhanced the IL-10/STAT3 axis, providing mechanistic insight into their cooperative inhibitory roles. Furthermore, we demonstrate that phosphotyrosine mimetic inhibitors of PTPN1, which were already found to be safe in humans, can be repurposed for cancer immunotherapy. This strategy can be used to increase the efficacy of PD-1 blockade and broaden its use to other cancer types.
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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.