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Publication
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Title of Article |
OPCML Exerts Antitumor Effects in Cholangiocarcinoma via
AXL/STAT3 Inactivation and Rho GTPase Down-regulation |
Date of Acceptance |
12 October 2021 |
Journal |
Title of Journal |
Cancer Genomics & Proteomics |
Standard |
ISI |
Institute of Journal |
International Institute of Anticancer Research |
ISBN/ISSN |
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Volume |
2021 |
Issue |
18 |
Month |
November-December |
Year of Publication |
2022 |
Page |
771-780 |
Abstract |
Background/Aim: Opioid-binding protein/cell
adhesion molecule-like (OPCML) plays a crucial role in the
suppression of tumor progression in several cancer types.
Nevertheless, the association between OPCML functions and
cholangiocarcinoma (CCA) progression remains unknown. We
aimed to investigate biological functions of OPCML and
related signaling pathways in CCA cell lines. Materials and
Methods: Methylation status and ectopic expression of
OPCML were determined in CCA cell lines using methylationspecific
polymerase chain reaction and pcDNA3.1+/C-
(K)DYK-OPCML, respectively. Cell proliferation, migration
and invasion were investigated. Results: OPCML was found
to be epigenetically silenced by DNA methylation. Ectopic
expression of OPCML inhibited CCA proliferation by inducing
apoptosis via AXL receptor tyrosine kinase/signal transducer
and activator of transcription 3 (AXL/STAT3) inactivation. It
also suppressed cell migration and invasion via downregulation
of Rho GTPases, ras homolog family member A
(RHOA), Rac family small GTPase 1 (RAC1) and cell division
cycle 42 (CDC42). Conclusion: We are the first to unravel the
antitumor effects and the related signaling pathways of
OPCML in CCA. The loss of OPCML expression due to
promoter hypermethylation can cause a decrease in cell death
but increase in cell migration and invasion, which may at least
in part contribute to CCA progression. |
Keyword |
OPCML, methylation, AXL/STAT3 signaling, RHOA/RAC1/CDC42 |
Author |
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Reviewing Status |
ไม่มีผู้ประเมินอิสระ |
Status |
ตีพิมพ์แล้ว |
Level of Publication |
นานาชาติ |
citation |
true |
Part of thesis |
true |
Attach file |
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