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PID1 increases chemotherapy-induced apoptosis in medulloblastoma and glioblastoma cells in a manner that involves

Jingying Xu1, Xiuhai Ren1, Anup Singh Pathania1

  • 1Saban Research Institute at Children's Hospital Los Angeles, Division of Hematology, Oncology and Blood & Marrow Transplantation, Department of Pediatrics, Los Angeles, California, 90027, USA.

Scientific Reports
|April 13, 2017
PubMed

Insights

Phosphotyrosine Interaction Domain containing 1 (PID1) enhances chemotherapy-induced apoptosis in brain tumors like medulloblastoma and glioblastoma. PID1 is crucial for etoposide and cisplatin effectiveness, potentially improving patient treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Phosphotyrosine Interaction Domain containing 1 (PID1) is a protein that inhibits the growth of various brain tumor cell lines.
  • Elevated PID1 mRNA levels correlate with improved survival in medulloblastoma and glioma patients, suggesting a role in therapeutic sensitivity.

Purpose of the Study:

  • To investigate the hypothesis that PID1 sensitizes brain tumors to chemotherapy.
  • To elucidate the mechanisms by which PID1 influences apoptosis induced by common chemotherapeutic agents.

Main Methods:

  • Utilized medulloblastoma and glioblastoma cell lines to assess PID1's role in apoptosis.
  • Employed siRNA to knock down PID1 expression and NFκB inhibitors (JSH-23, Bay117082) to study pathway involvement.
  • Investigated the role of proteasomal degradation using bortezomib.

Main Results:

  • PID1 significantly increased apoptosis induced by cisplatin and etoposide.
  • PID1 was essential for cisplatin-induced apoptosis, as shown by siRNA experiments.
  • Both etoposide and cisplatin activated NFκB signaling, which in turn regulated PID1 expression.
  • Etoposide upregulated PID1 via NFκB, while cisplatin led to proteasome-dependent PID1 degradation.

Conclusions:

  • PID1 plays a critical role in mediating apoptosis induced by etoposide and cisplatin in medulloblastoma and glioblastoma.
  • The findings highlight the involvement of NFκB signaling and proteasomal degradation in PID1-mediated chemo-sensitivity.
  • PID1 may serve as a predictive biomarker or therapeutic target for improving chemotherapy responsiveness in brain tumors.

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