Publication: RNA-binding protein DND1 participates in migration, invasion, and EMT of prostate cancer cells by degrading CLIC4
Authors
Zhang, Wei ; Xu, Qian ; Shi, Chunmei ; Chen, Xinfeng ; Shen, Cheng ; Zhang, Yong ; Zheng, Bing ; Zhu, Hua
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Publisher
Universidad de Murcia. Departamento de BiologĂa Celular e HistologĂa
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DOI
https://doi.org/10.14670/HH-18-720
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info:eu-repo/semantics/article
Description
Abstract
Dead-End 1 (DND1) is an RNA-binding
protein (RBP) with regulatory functions in multiple
cancers, including gastric and colorectal. Nevertheless,
the role that DND1 plays in prostatic cancer (PCa) as
well as the hidden molecular mechanism is still obscure.
The gene expression of DND1 and survival analyses in
PCa were analyzed by the UALCAN database.
Expression of DND1 and chloride intracellular channel 4
(CLIC4) were detected by qRT-PCR and western blot
analysis. The Cell Counting Kit-8 assay and EDU
staining were employed for the estimation of cell
viability. The capabilities of cells to migrate and invade
were appraised by the wound healing assay as well as
the Transwell assay, while epithelial-mesenchymal
transition (EMT) was measured by immunofluorescence
and western blot assay. The interaction of DND1 and
CLIC4 was predicted by PCTA, linkedomics, and
RPISeq databases. It was discovered that DND1
expression was elevated in PCa cells. DND1 silencing
had suppressive impacts on the proliferative, migrative,
and invasive capabilities as well as EMT in DU145 and
22Rv1 cells. Mechanistically, bioinformatic analysis
demonstrated that DND1 was negatively correlated with
CLIC4 and that DND1 protein could bind to CLIC4
mRNA. Additionally, the CLIC4 level was reduced in
PCa cells. CLIC4 depletion countervailed the
suppressive impacts of DND1 deficiency on the
capabilities of DU145 and 22Rv1 cells to proliferate,
migrate, and invade as well as the process of EMT.
These results suggested that DND1 silencing repressed
the proliferation, migration, invasion, and EMT in PCa
by regulating the mRNA level of CLIC4.
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Citation
Histology and Histopathology, Vol.39, nÂş10, (2024)
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