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PTPN2 deficiency along with activation of nuclear Akt predict endocrine resistance in breast cancer

Elin Karlsson1, Cynthia Veenstra2, Jon Gårsjö1

  • 1Department of Clinical and Experimental Medicine, Department of Oncology, Linköping University, 58185, Linköping, Sweden.

Journal of Cancer Research and Clinical Oncology
|December 6, 2018
PubMed
Abstract

Insights

Loss of protein tyrosine phosphatase, non-receptor type 2 (PTNP2) in breast cancer correlates with poor tamoxifen response. Low PTNP2 and high activated Akt indicate reduced endocrine treatment efficacy, suggesting potential for tailored therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Protein tyrosine phosphatase, non-receptor type 2 (PTNP2) is crucial in regulating receptor tyrosine kinase signaling.
  • PTNP2 normally inhibits intracellular pathways like PI3K/Akt.
  • The PTNP2 gene is located on chromosome 18p11, a region frequently deleted in breast cancer.

Purpose of the Study:

  • To assess PTNP2 protein expression in a large breast cancer cohort.
  • To investigate associations between PTNP2 expression, gene copy loss, and Akt activation.
  • To evaluate PTNP2 as a potential clinical marker in breast cancer.

Main Methods:

  • Immunohistochemistry was used to analyze PTNP2 protein expression in 664 node-negative breast tumors.
  • Real-time PCR determined PTNP2 gene copy number in a subset of 146 patients.
  • Akt activation was assessed by measuring nuclear-activated Akt (pAkt-n).

Main Results:

  • PTNP2 gene loss was observed in 17.8% of the tumors.
  • Low PTNP2 protein expression correlated with increased nuclear-activated Akt (pAkt-n).
  • Both low PTNP2 expression and the combination of low PTNP2/high pAkt-n predicted poor response to tamoxifen.

Conclusions:

  • PTNP2 negatively regulates Akt signaling in breast cancer.
  • Loss of PTNP2 protein expression, coupled with elevated pAkt-n, serves as a novel predictive marker for endocrine treatment efficacy.
  • These findings may facilitate personalized patient therapies in breast cancer treatment.
Keywords:
18p deletionBreast cancerGene copy numberImmunohistochemistryPTPN2Protein tyrosine phosphataseTCPTP

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