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Updated: Nov 23, 2025

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
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SHP-2 Interacts with CD81 and Regulates the Malignant Evolution of Colorectal Cancer by Inhibiting

Huaqin Yuan1, Jun Zhao2, Yang Yang3

  • 1Department of Oncology, Nanjing Gaochun People's Hospital Affiliated to Yangzhou University, Nanjing, Jiangsu 211316, People's Republic of China.

Cancer Management and Research
|December 31, 2020
PubMed
Abstract

Insights

Protein tyrosine phosphatase SHP-2 inhibits colon cancer progression by interacting with CD81. This study clarifies SHP-2

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Colon cancer is a prevalent digestive system malignancy.
  • Understanding the molecular mechanisms regulating colon cancer is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of protein tyrosine phosphatase SHP-2 in colon cancer.
  • To identify key targets and molecular mechanisms underlying SHP-2's regulation of colon cancer.

Main Methods:

  • Quantitative Real-time PCR (qRT-PCR) to assess SHP-2 expression in various tissues and cell lines.
  • Cellular assays (proliferation, Transwell, scratch, apoptosis) to evaluate SHP-2's functional impact.
  • Immunoprecipitation to identify SHP-2 interacting proteins, specifically CD81.

Main Results:

  • SHP-2 expression was significantly decreased in colon cancer tissues and cells compared to normal counterparts.
  • Overexpression of SHP-2 suppressed colon cancer cell proliferation, adhesion, and metastasis while promoting apoptosis.
  • SHP-2 was found to interact with CD81, inhibiting its function, and CD81 overexpression reversed SHP-2's anti-cancer effects.

Conclusions:

  • SHP-2 overexpression inhibits colon cancer progression through interaction with CD81.
  • This study elucidates the molecular mechanism of SHP-2 in colon cancer.
  • Findings offer potential guidance for colon cancer diagnosis and prognosis assessment.
Keywords:
CD81EMTSHP-2colorectal cancer

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