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Walleye dermal sarcoma virus Orf B functions through receptor for activated C kinase (RACK1) and protein kinase C

Candelaria C Daniels1, Joel Rovnak, Sandra L Quackenbush

  • 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO 80523, USA.

Virology
|March 18, 2008
PubMed

Insights

Walleye dermal sarcoma virus accessory proteins Orf A and Orf B may drive cancer. Orf B interacts with RACK1 and protein kinase C (PKC), promoting cell survival and proliferation.

Area of Science:

  • Virology
  • Oncology
  • Cell Biology

Background:

  • Walleye dermal sarcoma virus causes seasonal skin tumors in walleye.
  • Accessory gene transcripts A and B, and their encoded proteins Orf A and Orf B, are implicated in oncogenesis.
  • Tumor development correlates with low transcript levels, suggesting a critical role for these proteins.

Purpose of the Study:

  • To investigate the role of walleye dermal sarcoma virus Orf B protein in oncogenesis.
  • To identify cellular proteins interacting with Orf B.
  • To elucidate the mechanism by which Orf B influences cell behavior.

Main Methods:

  • Localization studies of Orf B in explanted tumor cells and mammalian cells.
  • Yeast two-hybrid assays and cell culture to identify Orf B interacting proteins.
  • Sequence analysis of walleye RACK1.
  • Investigation of Orf B association with protein kinase C (PKC) and the effects of activated PKC.

Main Results:

  • Orf B protein localizes to the cell periphery, similar to focal adhesions and actin stress fibers.
  • The cellular protein receptor for activated C kinase 1 (RACK1) binds to Orf B.
  • Walleye RACK1 is highly conserved.
  • Orf B associates with constitutively activated PKCalpha at the membrane.
  • Activated PKC signaling in Orf B-expressing cells promotes cell survival, proliferation, and viability.

Conclusions:

  • Orf B protein plays a significant role in walleye dermal sarcoma oncogenesis.
  • Orf B interacts with RACK1 and PKC, hijacking cellular signaling pathways.
  • The Orf B-RACK1-PKC interaction promotes cancer cell survival and proliferation, offering potential therapeutic targets.

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