TUSC3 loss alters the ER stress response and accelerates prostate cancer growth in vivo

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Updated: May 3, 2026

Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

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Peter Horak1, Erwin Tomasich1, Petr Vaňhara2

  • 1Division of Oncology, Department of Internal Medicine I and Comprehensive Cancer Center Medical University of Vienna, Austria.

Scientific Reports
|January 18, 2014
PubMed

Insights

Tumor suppressor candidate 3 (TUSC3) is crucial for regulating prostate cancer cell growth and invasion. Loss of TUSC3 impairs N-linked glycosylation and endoplasmic reticulum function, promoting cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prostate cancer is a leading malignancy in developed nations.
  • Tumor suppressor candidate 3 (TUSC3) is implicated in prostate cancer but its function is unknown.
  • TUSC3 homology to yeast Ost3p suggests a role in protein glycosylation.

Purpose of the Study:

  • To elucidate the function of TUSC3 in prostate cancer.
  • To investigate TUSC3's role in N-linked glycosylation and cellular processes.
  • To understand the mechanistic link between TUSC3, endoplasmic reticulum stress, and cancer signaling.

Main Methods:

  • Assessed TUSC3's role in the oligosaccharyltransferase (OST) complex.
  • Examined the impact of TUSC3 loss on prostate cancer cell proliferation, migration, and invasion.
  • Analyzed effects on xenograft growth, endoplasmic reticulum structure, stress response, and Akt signaling.

Main Results:

  • TUSC3 is confirmed as a component of the mammalian OST complex, influencing N-linked glycosylation.
  • TUSC3 downregulation in DU145 and PC3 cells increased proliferation, migration, invasion, and xenograft growth.
  • TUSC3 loss disrupted ER structure, heightened ER stress, and elevated Akt signaling.

Conclusions:

  • TUSC3 functions as a tumor suppressor in prostate cancer by regulating N-linked glycosylation.
  • TUSC3 deficiency promotes prostate cancer progression through ER stress and altered Akt signaling.
  • This study provides the first mechanistic insights into TUSC3's role in prostate carcinogenesis and N-glycosylation.

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