Publication: Downregulation of desmoglein 2 promotes EMT progression in gallbladder cancer
Authors
Wang, LingLing ; Lv, You ; Li, JinBin ; Nan, YongShan ; Piao, LongZhen ; Liang, ZheLong
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-535
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info:eu-repo/semantics/article
Description
Abstract
Objective. To explore the correlation
between the expression level of Desmoglein 2 (DSG2)
and the epithelial-mesenchymal transition (EMT)
progression in gallbladder cancer (GBC).
Method. 106 GBC tissue specimens and
corresponding clinical information were collected to
make a tissue microarray. Immunohistochemical method
was used to test the expression level of DSG2 in GBC
tissues. DSG2 was knocked down in the GBC cell line
GBC-SD to detect the change of its invasion and
metastasis ability. Then RT-qPCR and Western Blot were
applied on the DSG2-knocked down GBC-SD cells to
detect the expression level change of genes associated
with EMT.
Result. The high expression rate of DSG2 was
significantly correlated with the N, M and TNM staging
of patients (P<0.05). Survival analysis identified that
GBC patients with high DSG2 expression level had
significantly better survival (P<0.05). To further
investigate the potential mechanism of DSG2 on
regulating GBC tumor progression, we used knockdown
DSG2 on GBC-SD cell lines. The results showed that
GBC-SD cell lines with DSG2 knockdown showed a
promotion of cell invasion and metastatic ability. The
mRNA levels of EMT-related genes E-Cadherin, Snail,
Twist, ZEB1, and β-catenin, which is a key protein in the
Wnt signaling pathway, were also significantly altered.
Besides, protein levels of E-cadherin and Snail showed
consistent results.
Conclusion. The downregulation of DSG2 in
gallbladder cancer is hypothesized to be associated with
the invasion and metastasis progression of gallbladder
cancer cells by regulating EMT-related pathways. Its
expression level can be a novel biomarker for
gallbladder cancer, providing new perspectives for
diagnosis and treatment strategies.
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Citation
Histology and Histopathology Vol. 38, nº4 (2023)
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