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Related Experiment Video

Updated: Jan 7, 2026

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
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SHP2: A Redox-Sensitive Regulator Linking Immune Checkpoint Inhibitor Therapy to Cancer Treatment and Vascular Risk.

Silvia Fernanda López Moreno1,2, Stefania Assunto Lenz1,2, Bernardo Casso-Chapa1,2

  • 1Department of Cardiology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1057, Houston, TX 77030, USA.

Antioxidants (Basel, Switzerland)
|December 30, 2025
PubMed
Summary

Src homology 2-domain containing protein tyrosine phosphatase 2 (SHP2) plays a dual role in immune and vascular systems. Understanding its context-specific signaling is crucial for cancer therapy and managing cardiovascular complications from immune checkpoint inhibitors.

Keywords:
ICIPD-1PD-L1SHP2 tyrosine phosphataseand cardiovascular diseasecanceroxidative stressscaffold protein

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Last Updated: Jan 7, 2026

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Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Biology

Background:

  • Src homology 2-domain containing protein tyrosine phosphatase 2 (SHP2), encoded by PTPN11, is a critical mediator of PD-1/PD-L1 signaling.
  • SHP2's role extends beyond immune modulation to tumor development and vascular homeostasis, making it a significant therapeutic target.
  • The association between immune checkpoint inhibitors (ICIs), immune-related adverse events (irAEs), and cardiovascular complications highlights the need to elucidate SHP2's function in these processes.

Purpose of the Study:

  • To review current knowledge on SHP2/PTPN11 biology, its involvement in immune regulation, cancer, and vascular homeostasis.
  • To discuss emerging therapeutic strategies targeting the SHP2 pathway, particularly in combination with ICIs.
  • To explore the context-dependent and opposing signaling roles of SHP2 in different cellular environments.

Main Methods:

  • Literature review and synthesis of existing research on SHP2 function.
  • Analysis of SHP2's role in immune cells (T cells) and non-immune cells (endothelial cells, myeloid cells, vascular smooth muscle cells).
  • Examination of SHP2 signaling in response to various stimuli including PD-1/PD-L1, oxidative stress, radiation, and Notch-Jag1 signaling.

Main Results:

  • SHP2 conveys PD-1 mediated inhibitory signaling in T cells and is a target for improving ICI efficacy.
  • SHP2 promotes vascular homeostasis and inhibits inflammation in endothelial and myeloid cells under normal conditions.
  • SHP2 exhibits context-dependent opposing effects: promoting inflammation under oxidative stress but increasing fibrosis post-radiation; acting pro-atherogenically in vascular smooth muscle cells.

Conclusions:

  • SHP2's dual signaling capacity significantly modulates both immune and vascular system responses, influenced by redox state, cell type, and subcellular compartment.
  • Targeting SHP2 with ICIs is a promising strategy to overcome ICI resistance and enhance anti-tumor activity.
  • Further research is essential to mitigate SHP2-associated cardiovascular toxicity, especially in patients undergoing ICI treatment.