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Updated: Apr 12, 2026

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
Published on: July 17, 2020
Inhibition of SHP-2 promotes radiosensitivity in glioma
Quanye Sun1, Luyan Mu1, Wanchen Qiao1
1Department of Neurosurgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Abstract:
As a phosphatase, SHP-2 has been identified to be involved in regulating several cell functions, including growth, division, adhesion and motility. Therefore, SHP‑2 may affect the response of glioma to radiotherapy, such as via enhancing angiogenesis. The present study aimed to investigate the function of SHP‑2, a protein tyrosine phosphatase, in the radiosensitivity of glioma. U251, U87 and SHG44 glioma cell lines were transfected with small interfering (si)RNA against SHP‑2 and cell proliferation was assessed using a cell counting kit 8 assay, cell apoptosis was assessed by fluorescence‑activated cell sorting and immunoblotting, cell invasion was determined by an invasion assay, and the vasculogenic mimicry capacity was assessed by a tube formation assay. SHP‑2 siRNA transfection reduced the proliferation and increased apoptosis in the glioma cell lines. Downregulation of SHP‑2 suppressed glioma cell invasion and vasculogenic mimicry. These results demonstrated that no significant difference was observed between glioma tissues and normal brain tissues, however, silencing of SHP‑2 inhibited cell proliferation, invasion and vasculogenic mimicry in the glioma cell lines. SHP‑2 may be a novel therapeutic target for glioma.
Insights
Silencing SHP-2 (a protein tyrosine phosphatase) inhibits glioma cell proliferation, invasion, and vasculogenic mimicry, suggesting it is a potential therapeutic target for glioma radiosensitivity.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- SHP-2 is a protein tyrosine phosphatase regulating cell functions like growth, division, adhesion, and motility.
- SHP-2's role in angiogenesis suggests it may influence glioma response to radiotherapy.
- Understanding SHP-2's function is crucial for developing targeted glioma therapies.
Purpose of the Study:
- To investigate the function of SHP-2 in the radiosensitivity of glioma.
- To determine if SHP-2 plays a role in glioma cell proliferation, apoptosis, invasion, and vasculogenic mimicry.
Main Methods:
- Glioma cell lines (U251, U87, SHG44) were transfected with small interfering RNA (siRNA) targeting SHP-2.
- Cell proliferation was assessed using a cell counting kit 8 assay.
- Apoptosis was evaluated by fluorescence-activated cell sorting and immunoblotting.
- Cell invasion and vasculogenic mimicry were assessed using invasion and tube formation assays, respectively.
Main Results:
- SHP-2 siRNA transfection significantly reduced proliferation and increased apoptosis in glioma cell lines.
- Downregulation of SHP-2 suppressed glioma cell invasion and vasculogenic mimicry.
- No significant difference in SHP-2 expression was observed between glioma and normal brain tissues.
Conclusions:
- SHP-2 downregulation inhibits key malignant behaviors in glioma cells, including proliferation, invasion, and vasculogenic mimicry.
- SHP-2 plays a significant role in glioma radiosensitivity.
- SHP-2 represents a potential novel therapeutic target for glioma treatment.
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