Publication: Mechanism of lncRNA PLACT1 in regulating the proliferation of pancreatic adenocarcinoma cells through the KLF2/KIAA1522 axis
Authors
Xiaoli Hou ; Shutao Wu ; Wei Sun ; Yixia Wang ; Yasen Cao ; Hong Cheng ; Fei Wang
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Publisher
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Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-25-011
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info:eu-repo/semantics/article
Description
Abstract
Background. Pancreatic adenocarcinoma
(PAAD) is among the most common cancers worldwide.
This study aims to investigate the role of long noncoding
RNA pancreatic cancer-associated transcript 1 (LncRNA
PLACT1) in PAAD cell proliferation.
Methods. PAAD and normal cells were cultured. The
levels of PLACT1, Krüppel-like factor 2 (KLF2), and
KIAA1522 were detected. After PLACT1 expression
was interfered with, cell proliferation was detected using
the cell counting kit-8, clone formation assay, and 5
ethynyl-2-deoxyuridine (EdU) staining. The binding of
PLACT1 to euchromatic histone lysine methyl
transferase 2 (EHMT2) was analyzed. The enrichment of
EHMT2 and histone H3 lysine 9 dimethylation
(H3K9me2) on the KLF2 promoter was analyzed by
chromatin immunoprecipitation. KLF2 expression was
detected after EHMT2 intervention. The binding of
KLF2 to the KIAA1522 promoter was analyzed. The
nude mouse xenograft model was constructed to detect
the role of PLACT1 in vivo.
Results. PLACT1 and KIAA1522 were highly
expressed, and KLF2 was poorly expressed in PAAD
cells. Silencing PLACT1 decreased cell proliferation, the
number of cell clones, and EdU-positive cells.
Mechanistically, PLACT1 inhibited KLF2 expression by
recruiting EHMT2 to induce H3K9me2 in the KLF2
promoter region, resulting in reduced KLF2 enrichment
at the KIAA1522 promoter and increased KIAA1522
expression. KLF2 downregulation or KIAA1522
overexpression alleviated the inhibitory effect of
PLACT1 silencing on PAAD cell proliferation. PLACT1 silencing prevented PAAD tumorigenesis by regulating
the KLF2/KIAA1522 pathway.
Conclusion. PLACT1 silencing inhibited PAAD by
inhibiting KLF2 and promoting KIAA1522 expression,
suggesting the therapeutic effect of PLACT1 silencing
on PAAD.
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