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\title{SFQP regulates CTL mediated cytotoxicity on NSCLC by directly binding to
PD-L1 3'UTR}



\author[1]{Yanming Pan}%
\author[1]{Yongxia Cheng}%
\affil[1]{Mudanjiang Medical University}%


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  \date{April 27, 2026}


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\begin{abstract}
Splicing factor proline- and glutamine-rich (SFPQ) can interact with
RNAs to regulate gene expression. The function of SFPQ in the
immunotherapy of non-small cell lung cancer (NSCLC) is investigated in
this study. H1299 and A549 cells were transfected with shSFPQ plasmid.
Cell counting kit-8 (CCK-8) and cell clone formation were utilized to
detect survival and proliferation. Programmed death-ligand 1 (PD-L1) and
SFPQ were detected in NSCLC patients treated with anti-PD-L1 antibody.
Dual-luciferase assays, RNA immunoblotting, RNA pull-down, and mRNA
stability assay were applied to verify the regulation of PD-L1 with
SFPQ. Human peripheral blood mononuclear cells (PBMC)-derived dendritic
cells were loaded with irradiated A549 and H1299 cells, which were
cultured with autologous CD8+T cells and tumor cells to perform in vitro
tumor-specific cytotoxic T cells (CTL) cytotoxicity analysis. SFPQ
silencing inhibited the survival and proliferation of H1299 and A549
cells with down-regulated PD-L1 expression. PD-L1 and SFPQ expression
were markedly higher in anti-PD-L1 antibody treatment responders
compared to non-responders, which showed a positive Pearson correlation
(r=0.76, p\textless{}0.001). SFPQ up-regulated the relative mRNA and
protein expression of PD-L1 by binding to the PD-L1 3'UTR to slow the
decay of PD-L1 mRNA. SFPQ silencing promoted the killing effect of CTL
on A549 and H1299 cells. SFQP up-regulates PD-L1 expression by binding
with PD-L1 3'UTR to slow the decay of PD-L1 mRNA, and SFQP silencing
promotes CTL mediated cytotoxicity on NSCLC cells.%
\end{abstract}%



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