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Last update 08 May 2025

PTPN3

Last update 08 May 2025

Basic Info

Synonyms

protein tyrosine phosphatase non-receptor type 3, Protein-tyrosine phosphatase H1, PTP-H1

+ [3]

Introduction

May act at junctions between the membrane and the cytoskeleton. Possesses tyrosine phosphatase activity.

Drugs associated with PTPN3

CN116814757

Patent Mining

Target

PTPN3

Mechanism-

Active Org.

Shihezi University

Originator Org.

Shihezi University

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PTPN3

100 Translational Medicine associated with PTPN3

0 Patents (Medical) associated with PTPN3

121

Literatures (Medical) associated with PTPN3

01 Apr 2024·Journal of Immunotherapy

Inhibition of PTPN3 Expressed in Activated Lymphocytes Enhances the Antitumor Effects of Anti-PD-1 Therapy in Head and Neck Cancer, Especially in Hypoxic Environments

Article

Author: Masuda, Shogo ; Nagao, Shinjiro ; Koga, Satoko ; Imaizumi, Akira ; Onishi, Hideya ; Iwamoto, Naoya ; Kogo, Ryunosuke ; Umebayashi, Masayo ; Morisaki, Takashi ; Komune, Noritaka ; Itoyama, Shinsaku ; Sakanashi, Keita ; Fujimura, Akiko ; Nakagawa, Takashi

In the tumor microenvironment, wherein cytotoxic lymphocytes interact with cancer cells, lymphocyte exhaustion, an immune checkpoint inhibitor target, is promoted. However, the efficacy of these inhibitors is limited, and improving response rates remains challenging. We previously reported that protein tyrosine phosphatase nonreceptor type (PTPN) 3 is a potential immune checkpoint molecule for activated lymphocytes and that PTPN3 inhibition should be a focus area for cancer immunotherapy development. Therefore, in this study, we focused on PTPN3-suppressive therapy in terms of lymphocyte exhaustion under hypoxic conditions, which are a cancer microenvironment, and investigated measures for improving the response to anti-programmed death receptor (PD)-1 antibody drugs. We found that PTPN3 expression was upregulated in activated lymphocytes under hypoxic conditions, similar to the findings for other immune checkpoint molecules, such as PD-1, T cell immunoglobulin mucin-3, and lymphocyte-activation gene-3; furthermore, it functioned as a lymphocyte exhaustion marker. In addition, PTPN3-suppressed activated lymphocytes promoted the mammalian target of rapamycin (mTOR)-Akt signaling pathway activation and enhanced proliferation, migration, and cytotoxic activities under hypoxic conditions. Furthermore, PTPN3 suppression in activated lymphocytes increased PD-1 expression and enhanced the antitumor effects of anti-PD-1 antibody drugs against head and neck cancer in vitro and in vivo. These results suggest that the suppression of PTPN3 expression in activated lymphocytes enhances the therapeutic effect of anti-PD-1 antibody drugs in head and neck cancer, especially under hypoxic conditions that cause lymphocyte exhaustion.

28 Mar 2024·Modern Rheumatology

Extraction of characteristic serum microRNAs and prediction of target genes in IgG4-related dacryoadenitis and sialadenitis

Article

Author: Kamekura, Ryuta ; Yamamoto, Motohisa ; Aochi, Satsuki ; Tanaka, Tomonao ; Uehara, Masaaki ; Takano, Ken-Ichi

ABSTRACTObjectivesTo identify the specific microRNAs (miRNAs) in IgG4-related dacryoadenitis and sialadenitis (IgG4-DS) and predict the targeted genes.MethodsmiRNAs in the serum of nine patients with IgG4-DS, three patients with primary Sjögren’s syndrome, and three healthy controls were analysed using the human miRNA chip, and miRNAs that exhibited significant fluctuation in expression in IgG4-DS patients were extracted. The respective target genes were predicted using an existing database, and expression of the target genes was evaluated in actual submandibular gland tissues affected by IgG4-DS.ResultsSerum miR-125a-3p and miR-125b-1-3p levels were elevated in IgG4-DS. Six candidate target genes (glypican 4, forkhead box C1, protein tyrosine phosphatase non-receptor type 3, hydroxycarboxylic acid receptor 1, major facilitator superfamily domain containing 11, and tumour-associated calcium signal transducer 2) were downregulated in the affected submandibular gland tissue.ConclusionOverexpression of miR-125a-3p and miR-125b-1-3p is a hallmark of IgG4-DS. These miRNAs appear to be involved in the pathogenesis of IgG4-DS.

01 Nov 2023·Journal of cancer research and clinical oncology

PTPN3 inhibition contributes to the activation of the dendritic cell function to be a promising new immunotherapy target.

Article

Author: Nagao, Shinjiro ; Sakanashi, Keita ; Morisaki, Takashi ; Onishi, Hideya ; Nakamura, Masafumi ; Morisaki, Shinji ; Iwamoto, Naoya ; Umebayashi, Masayo ; Ozono, Keigo ; Koga, Satoko ; Imaizumi, Akira ; Masuda, Shogo

PURPOSEIn a previous study, protein tyrosine phosphatase non-receptor type (PTPN) 3 was identified as an immune checkpoint molecule in lymphocytes, and its potential as a novel target for cancer immunotherapy was anticipated. However, evaluation of dendritic cell (DC) function as antigen-presenting cells is critical for the development of immunotherapy. In this study, we aimed to analyze the biological effect of PTPN3 on DCs induced from human peripheral blood monocytes obtained from healthy individuals.METHODSWe used short-interfering RNA to knock down PTP3 in DCs. For DC maturation, we added cancer cell lysate and tumor necrosis factor-α/interferon-α to immature DCs. In the cytotoxic assay, the target cancer cells were SBC5, unmatched with DCs from healthy human leukocyte antigen (HLA)-A24, or Sq-1, matched with DCs. Enzyme-linked immunosorbent assay was used to determine the amount of cytokines. To examine the intracellular signaling system, intracellular staining was used.RESULTSPTPN3 knockdown significantly increased the number of DCs, expression of CD80 and chemokine receptor (CCR)7, and production of interleukin-12p40/p70 in mature DCs. In the HLA-A24-restricted DC and human lung squamous cell carcinoma cell cytotoxic assay, inhibition of PTPN3 expression in mature DCs induced cytotoxic T lymphocytes with increased production of INF-γ and granzyme B, and enhanced toxicity against cancer cells and migration to cancer. Furthermore, inhibition of PTPN3 expression activated the mitogen-activated protein kinase pathway in DCs.CONCLUSIONBased on our findings, inhibition of PTPN3 expression could contribute to the development of novel cancer immunotherapies that activate not only lymphocytes but also DCs.

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PTPN3

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