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Targeting SHP1 and SHP2 to suppress tumors and enhance immunosurveillance

Yijun Zhao1, Linjia Jiang1

  • 1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510000, China.

Trends in Cell Biology
|November 22, 2024
PubMed

Insights

SHP1 and SHP2 phosphatases regulate immune signaling and cancer. Inhibitors of these phosphatases show promise in improving cancer therapies by boosting chemotherapy and immune responses.

Area of Science:

  • Biochemistry
  • Immunology
  • Oncology

Background:

  • Nonreceptor tyrosine phosphatases SHP1 and SHP2 dephosphorylate substrates in receptor tyrosine kinase (RTK) and immune receptor signaling pathways.
  • These phosphatases are critical for maintaining signal transduction balance, impacting hematopoiesis, immune regulation, and tumor biology.

Purpose of the Study:

  • To review the functions of SHP1 and SHP2 in hematopoiesis, immune regulation, and cancer.
  • To highlight recent findings on SHP1/SHP2 in cancer-driven immune evasion.
  • To discuss the therapeutic potential of SHP1 and SHP2 inhibitors in cancer treatment.

Main Methods:

  • Literature review of research on SHP1 and SHP2 functions.
  • Analysis of studies on hematopoiesis, immune regulation, and tumor biology.
  • Examination of findings related to cancer immune evasion and therapeutic strategies.

Main Results:

  • SHP1 and SHP2 play key roles in regulating immune cell function and development.
  • Dysregulation of SHP1 and SHP2 is implicated in various cancers and immune evasion mechanisms.
  • SHP1 and SHP2 inhibitors enhance chemotherapy efficacy and augment anti-tumor immune responses.

Conclusions:

  • SHP1 and SHP2 are crucial regulators in immunity and cancer.
  • Targeting SHP1 and SHP2 with inhibitors represents a promising strategy to overcome cancer immune evasion and improve treatment outcomes.
Keywords:
SHP1SHP2chemoresistanceimmune checkpointimmunosurveillancereceptor tyrosine kinasesignal transductiontumorigenesis

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