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Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
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Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

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Phosphorylated 4EBP1 is associated with tumor progression and poor prognosis in Xp11.2 translocation renal cell

Yuanyuan Qu1,2, Rui Zhao3, Hongkai Wang1,2

  • 1Department of Urology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.

Scientific Reports
|March 31, 2016
PubMed

Insights

High p-4EBP1 expression in Xp11.2 renal cell carcinoma (RCC) correlates with poor prognosis and lymph node metastasis. Targeting 4E-BP1 phosphorylation may improve patient outcomes in this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • The PI3K-AKT-mTOR and RAS-MAPK pathways are crucial for cancer proliferation but their role in Xp11.2 renal cell carcinoma (RCC) is unclear.
  • Understanding these pathways is vital for developing targeted therapies for Xp11.2 RCC.

Purpose of the Study:

  • To investigate the expression of mTOR and MAPK pathway proteins in Xp11.2 RCC.
  • To determine the prognostic significance of these protein expressions in Xp11.2 RCC patients.

Main Methods:

  • Immunohistochemistry was used to assess the expression of 4EBP1, p-4EBP1, p-mTOR, p-S6K, and p-MAPK.
  • FISH assay confirmed Xp11.2 RCC in 36 adult patients.
  • Cox regression models were employed for prognostic analysis.

Main Results:

  • High expression of p-4EBP1 was observed in 72.2% of patients.
  • p-4EBP1 expression significantly correlated with lymph node metastasis (P = 0.027).
  • High p-4EBP1 expression independently predicted shorter Progression-Free Survival (PFS) (HR = 33.750, P = 0.017) and Overall Survival (OS) (HR = 56.111, P = 0.026).

Conclusions:

  • Phosphorylated 4E-BP1 (p-4EBP1) is a significant adverse prognostic factor in Xp11.2 RCC.
  • p-4EBP1 may act as a convergence point for oncogenic signaling.
  • Inhibiting pathways that phosphorylate 4E-BP1 could be a therapeutic strategy for Xp11.2 RCC.

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