Key result
ELAVL1 overexpression promotes MSB1 cell proliferation and inhibits apoptosis via the COX-2/PGE2 pathway.
Why the study?
ELAVL1 regulates tumor cell proliferation and apoptosis, but its role in Marek disease virus-induced oncogenesis remains unclear.
ELAVL1 promotes proliferation and inhibits apoptosis in MDV-transformed MSB1 cells, likely through the COX-2/PGE2 signaling pathway.
Should not yet change practice; hypothesis-generating for ELAVL1/COX-2/PGE2 axis in virally transformed cells.
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.
No takes yet. Share an insight, caveat, or question.
He et al. (2026) studied Marek's disease (MDV-induced oncogenesis). ELAVL1 overexpression or ELAVL1-specific siRNA vs. Control was evaluated on Cell proliferation, cell cycle distribution, apoptosis, and COX-2/PGE2 expression. ELAVL1 overexpression significantly promoted proliferation and inhibited apoptosis in MDV-transformed MSB1 cells, while ELAVL1 knockdown had the opposite effect, potentially via the COX-2/PGE2 pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: