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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Protein changes associated with ionizing radiation-induced apoptosis in human prostate epithelial tumor cells

S C Prasad1, V A Soldatenkov, M R Kuettel

  • 1Department of Radiation Medicine, Vincent T. Lombardi Cancer Center, Georgetown University Medical Center, Washington, DC 20007-2197, USA. prasads@gunet.georgetown.edu

Electrophoresis
|May 27, 1999
PubMed

Insights

Ionizing radiation (IR) therapy for prostate cancer causes cell death by altering protein levels. Key intermediate filament proteins decrease while chaperone proteins accumulate during IR-induced apoptosis.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Ionizing radiation (IR) is a crucial treatment for localized prostate cancer.
  • Understanding protein changes during IR-induced apoptosis is vital for comprehending cancer cell death.
  • Prostate cancer cells undergo programmed cell death (apoptosis) when exposed to IR.

Purpose of the Study:

  • To identify protein alterations during the execution phase of IR-induced apoptosis in prostate cancer cells.
  • To characterize the metabolic status of dying prostate cancer cells.
  • To investigate the role of intermediate filament proteins and molecular chaperones in IR-induced apoptosis.

Main Methods:

  • Utilized an in vitro model of radiation-transformed human prostate epithelial cells (267B1-XR).
  • Applied analytical two-dimensional polyacrylamide gel electrophoresis (2-D PAGE).
  • Confirmed protein changes using Western blotting with specific antisera.

Main Results:

  • Significant reduction in intermediate filament proteins (keratins-18, 19, vimentin) and 14-3-3 adapter proteins observed.
  • Marked accumulation of molecular chaperones (glucose-regulated protein 94, calreticulin, calnexin, protein disulfide isomerase) in dying cells.
  • Evidence of specific proteolysis solubilizing intermediate filaments and increased endoplasmic reticulum (ER) chaperone proteins.

Conclusions:

  • Apoptosis in prostate cancer cells involves the breakdown of intermediate filament networks.
  • Increased levels of ER chaperone proteins are associated with IR-induced cell death.
  • These protein profile changes provide insights into the cellular mechanisms of prostate cancer therapy response.

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