# ELAVL1 Promotes Proliferation and Inhibits Apoptosis of the Marek’s Disease Virus (MDV)-Transformed Cell Line MSB1 via the COX-2/PGE2 Pathway

## TL;DR

This study shows that ELAVL1 promotes cancer-like growth in chicken cells infected by Marek’s disease virus through the COX-2/PGE2 pathway.

## Contribution

The novel finding is that ELAVL1 contributes to MDV-induced oncogenesis via activation of the COX-2/PGE2 pathway in transformed cells.

## Key findings

- Overexpression of ELAVL1 increases proliferation and reduces apoptosis in MDV-transformed MSB1 cells.
- ELAVL1 activates the COX-2/PGE2 pathway, as evidenced by elevated COX-2 and PGE2 levels.
- Knockdown of ELAVL1 reverses these effects, inhibiting proliferation and decreasing COX-2/PGE2 expression.

## Abstract

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.

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.