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Viral-Mediated AURKB Cleavage Promotes Cell Segregation and Tumorigenesis

Qing Zhu1, Ling Ding1, Zhenguo Zi2

  • 1MOE and MOH Key Laboratory of Medical Molecular Virology, School of Basic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Cell Reports
|March 28, 2019
PubMed

Insights

Oncoviruses can cleave Aurora kinase B (AURKB), creating a fragment that promotes cancer cell division and tumor growth. This viral mechanism drives cancer progression by altering chromosome segregation.

Area of Science:

  • Molecular Biology
  • Oncology
  • Virology

Background:

  • Aurora kinase B (AURKB) is crucial for cell division and often dysregulated in cancer.
  • The role of AURKB in cancers associated with oncogenic viruses is not well understood.

Purpose of the Study:

  • To investigate the link between AURKB and oncogenic viruses in cancer progression.
  • To elucidate the mechanism by which oncoviruses affect AURKB function.

Main Methods:

  • Analysis of N-cleaved AURKB isoforms in oncovirus-associated tumor cells and patient tissues (KSHV, EBV, HPV).
  • Investigation of AURKB cleavage by the KSHV latent antigen LANA in infected cells.
  • Functional studies using N'-AURKB and C'-AURKB in vitro and in vivo (murine xenograft model).

Main Results:

  • N-cleaved AURKB isoforms were identified in tumors linked to KSHV, EBV, and HPV.
  • KSHV LANA was shown to cleave AURKB at Asp76 in a serine protease-dependent manner.
  • The N'-AURKB fragment localized to the spindle pole, promoting mitotic progression and enhancing tumor cell proliferation and malignant growth.

Conclusions:

  • Oncoviruses utilize proteolytic cleavage of AURKB as a mechanism to promote cancer cell segregation.
  • The viral induction of N'-AURKB contributes to tumorigenesis by enhancing malignant growth.
  • This study reveals a novel viral strategy impacting host cell division machinery for cancer development.
Keywords:
AURKBEBVHPVKSHVcell segregationoncovirusprotein cleavagetumorigenesis

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