ELAVL1 Promotes Proliferation and Inhibits Apoptosis of the Marek’s Disease Virus (MDV)-Transformed Cell Line MSB1 via the COX-2/PGE2 Pathway
by
, , and
Lei He
1,2,†,
Dong-Mei Zhan
1,2,†,
Hui Peng
1,2,
Meng-Ru Gao
1,2,
Jian Chen
1,2,
Yan-Yan Jia
1,2,
Cheng-Shui Liao
1,2,
Song-Biao Chen
1,2,
Ke Ding
1,2,3,* and
Zu-Hua Yu
1,2,* 1
Laboratory of Functional Microbiology and Animal Health, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China
2
Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Henan University of Science and Technology, Luoyang 471023, China
3
College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xingxiang 453003, China
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Animals 2026, 16(5), 843; https://doi.org/10.3390/ani16050843
Submission received: 15 January 2026
/
Revised: 26 February 2026
/
Accepted: 4 March 2026
/
Published: 7 March 2026
(This article belongs to the Special Issue Pathogenesis, Immunology and Epidemiology of Veterinary Viruses—2nd Edition)
Simple Summary
Marek’s disease virus (MDV) causes lymphoproliferative tumors in chickens. Although the RNA-binding protein ELAVL1 is implicated in tumorigenesis, its role in MDV-induced oncogenesis remains unclear. This study investigated the role of ELAVL1 in the MDV-transformed MSB1 cell line, specifically in the COX-2/PGE2 pathway. Overexpression of ELAVL1 significantly enhanced cell proliferation, promoted G1-to-S/G2 phase cell cycle progression, and reduced apoptosis. These changes were accompanied by upregulated transcription and expression of COX-2 and PGE2. Conversely, siRNA-mediated knockdown of ELAVL1 inhibited cell proliferation, induced G1 phase arrest, and decreased COX-2 and PGE2 expression. The findings suggest that the RNA-binding protein ELAVL1 enhances the oncogenic properties of MDV-transformed lymphocytes by activating the COX-2/PGE2 signaling pathway, unraveling the potential mechanism through which MDV induces oncogenesis.
Abstract
Marek’s disease (MD), caused by the oncogenic Marek’s disease virus (MDV), is a highly contagious avian infection that induces lymphoproliferative tumors. The RNA-binding protein ELAVL1 is known to regulate tumor cell proliferation and apoptosis, but its role in MDV-induced oncogenesis remains unclear. This study investigated whether ELAVL1 modulates proliferation and apoptosis in the MDV-transformed MSB1 cell line and whether its effects involve the cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathway. MSB1 cells were transiently transfected with ELAVL1-overexpressing plasmids (pEGFP-C-ELAVL1) or ELAVL1-specific siRNA, with expression confirmed by real-time PCR (qRT-PCR). Cell proliferation was assessed using the CCK-8 assay, while cell cycle distribution and apoptosis rates were analyzed by flow cytometry. COX-2 and PGE2 expression levels were determined by qRT-PCR, Western blotting, and ELISA. Overexpression of ELAVL1 significantly promoted the proliferation of MSB1 cells, decreased transition into the G1 phase, increased the proportions of S and G2 phase cells, and suppressed apoptosis. Correspondingly, both mRNA and protein levels of COX-2 and PGE2 were significantly elevated. Conversely, ELAVL1 knockdown significantly inhibited proliferation, induced G1 phase arrest, decreased S phase cells, and significantly decreased COX-2 and PGE2 expression. These findings indicate that ELAVL1 promotes proliferation and inhibits apoptosis in MDV-transformed MSB1 cells, potentially via the COX-2/PGE2 signaling pathway.
Keywords:
ELAVL1; Marek’s disease; MSB1; proliferation; apoptosis; COX-2/PGE2
