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The mechanism of the contribution of ICAM-1 to epithelial–mesenchymal transition (EMT) in bladder cancer
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The mechanism of the contribution of ICAM-1 to epithelial–mesenchymal transition (EMT) in bladder cancer
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Journal Article
The mechanism of the contribution of ICAM-1 to epithelial–mesenchymal transition (EMT) in bladder cancer
2024
Overview
Bladder cancer is one of the most prevalent cancers worldwide. Moreover, if not optimally treated, bladder cancer is a significant burden on healthcare systems due to multiple recurrences which often require more aggressive therapies. Therefore, targeted anti-cancer therapies, developed based on an in-depth understanding of specific proteins and molecular mechanisms, are promising in cancer treatment. Here, for the first time, we presented the new approaches indicating that intracellular adhesion molecule-1 (ICAM-1) may play a potential role in enhancing therapeutic effectiveness for bladder cancer. In the present study, we presented that ICAM-1 expression as well as its regulation in bladder cancer is strongly correlated with the high expression of N-cadherin. Importantly, the presence of N-cadherin and its regulator—TWIST-1 was abolished when ICAM-1 was silenced. We identified also that ICAM-1 is capable of regulating cellular migration, proliferation, and EMT progression in bladder cancer cells via the N-cadherin/SRC/AKT/GSK-3β/β-catenin signaling axis. Therefore, we propose ICAM-1 as a novel metastatic marker for EMT progression, which may also be used as a therapeutic target in bladder cancer.
Publisher
Springer Nature Singapore,Springer Nature B.V
Subject
/ Biomedical and Life Sciences
/ Epithelial-Mesenchymal Transition - genetics
/ Glycogen Synthase Kinase 3 beta
/ Humans
/ Intercellular adhesion molecule 1
/ Intercellular Adhesion Molecule-1 - genetics
/ Kinases
/ Oncology
/ Proteins
/ Software
/ Surgery
/ Urinary Bladder Neoplasms - genetics
/ Urinary Bladder Neoplasms - metabolism
