Viral-Mediated AURKB Cleavage Promotes Cell Segregation and Tumorigenesis
Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several o...
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| Published in | Cell reports (Cambridge) Vol. 26; no. 13; pp. 3657 - 3671.e5 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
26.03.2019
Elsevier |
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| Abstract | Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi’s sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp76 in a serine protease-dependent manner. The N′-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N′-AURKB but not C′-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis.
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•Cleaved AURKB exists in many oncovirus-related cancer cells and patient cancer tissue•Oncovirus-mediated AURKB cleavage occurs at Asp76 and relies on a serine protease•The N′-AURKB promotes the metaphase-to-telophase transition in mitotic cells•The N′-AURKB promotes tumor growth and malignancy in vitro and in vivo
Zhu et al. find that proteolytic cleavage of AURKB occurs in several oncovirus-associated cancer cells. Specifically, the oncovirus antigen LANA cleaves AURKB to promote the metaphase-to-telophase transition, thereby inducing host cell segregation and tumorigenesis. |
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| AbstractList | Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi's sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp
in a serine protease-dependent manner. The N'-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N'-AURKB but not C'-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis. Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi’s sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp76 in a serine protease-dependent manner. The N′-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N′-AURKB but not C′-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis. : Zhu et al. find that proteolytic cleavage of AURKB occurs in several oncovirus-associated cancer cells. Specifically, the oncovirus antigen LANA cleaves AURKB to promote the metaphase-to-telophase transition, thereby inducing host cell segregation and tumorigenesis. Keywords: AURKB, protein cleavage, KSHV, HPV, EBV, oncovirus, cell segregation, tumorigenesis Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi's sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp76 in a serine protease-dependent manner. The N'-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N'-AURKB but not C'-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis.Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi's sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp76 in a serine protease-dependent manner. The N'-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N'-AURKB but not C'-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis. Aurora kinase B (AURKB), a central regulator of chromosome segregation and cytokinesis, is aberrantly expressed in various cancer cells. However, the relationship of AURKB and oncogenic viruses in cancer progression remains unclear. Here, we reveal that N-cleaved isoforms of AURKB exist in several oncovirus-associated tumor cells and patient cancer tissues, including Kaposi’s sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human papillomavirus virus (HPV). Mechanistically, in KSHV-infected tumor cells, the latent viral antigen LANA cleaves AURKB at Asp76 in a serine protease-dependent manner. The N′-AURKB relocalizes to the spindle pole and promotes the metaphase-to-telophase transition in mitotic cells. Introduction of N′-AURKB but not C′-AURKB promotes colony formation and malignant growth of tumor cells in vitro and in vivo using a murine xenograft model. Altogether, our findings uncover a proteolytic cleavage mechanism by which oncoviruses induce cancer cell segregation and tumorigenesis. [Display omitted] •Cleaved AURKB exists in many oncovirus-related cancer cells and patient cancer tissue•Oncovirus-mediated AURKB cleavage occurs at Asp76 and relies on a serine protease•The N′-AURKB promotes the metaphase-to-telophase transition in mitotic cells•The N′-AURKB promotes tumor growth and malignancy in vitro and in vivo Zhu et al. find that proteolytic cleavage of AURKB occurs in several oncovirus-associated cancer cells. Specifically, the oncovirus antigen LANA cleaves AURKB to promote the metaphase-to-telophase transition, thereby inducing host cell segregation and tumorigenesis. |
| Author | Cai, Qiliang Wei, Fang Wang, Yuyan Gao, Shujun Wang, Chong Ding, Ling Zhu, Caixia Zhu, Qing Zi, Zhenguo Yuan, Zhenghong |
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| Keywords | oncovirus KSHV protein cleavage EBV cell segregation tumorigenesis AURKB HPV |
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| SubjectTerms | Adult Aged Animals AURKB Aurora Kinase B - metabolism Carcinogenesis cell segregation Chromosome Segregation EBV Female HEK293 Cells HeLa Cells Herpesvirus 8, Human - physiology HPV Humans KSHV Male Mice Mice, Inbred NOD Middle Aged Mitosis Neoplasms - metabolism Neoplasms - virology Oncogenic Viruses - physiology oncovirus protein cleavage tumorigenesis Xenograft Model Antitumor Assays Young Adult |
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| Title | Viral-Mediated AURKB Cleavage Promotes Cell Segregation and Tumorigenesis |
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