Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis

D Dipayan Bose (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania) N Nian Ma (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania) R Rajnish Kumar Singh (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania) R Ramakrishna Vangala (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania) A Atharva Torne (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania) K Kiran Chunduru (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania) E Erle S. Robertson (Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania)

Abstract

Never in mitosis A (NIMA)-related kinase 2 (NEK2) is a serine/threonine kinase that plays a crucial role in cell cycle regulation and is frequently induced across multiple cancer types, where its elevated levels are associated with poor prognosis. Epstein–Barr virus (EBV) and Kaposi’s sarcoma–associated herpesvirus (KSHV), both known to drive various malignancies, were observed to induce NEK2 expression during both primary infection and latent phases of infection. Increased NEK2 expression contributes to chromosomal instability by promoting nondisjunction, leading to a rise in aneuploid cell populations and fostering uncontrolled cell proliferation. Mechanistically, EBV latent protein EBNA2 and KSHV latent antigen LANA were identified as principal regulators of NEK2 upregulation, acting through modulation of RBP-Jκ activities at the NEK2 promoter region. Additionally, we demonstrated that targeting NEK2 impaired EBV- and KSHV-mediated tumor progression, highlighting its potential as a critical driver of virus-induced oncogenesis and a promising therapeutic target.

Article Details

Volume / Issue Vol. 123, Issue 9
Published March 03, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (7)

D

Dipayan Bose

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania

N

Nian Ma

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania

R

Rajnish Kumar Singh

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania

R

Ramakrishna Vangala

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania

A

Atharva Torne

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania

K

Kiran Chunduru

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania

E

Erle S. Robertson

Departments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, Tumor Virology Training Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania