ArticleHuman cell2024
The mechanism of the contribution of ICAM-1 to epithelial-mesenchymal transition (EMT) in bladder cancer.
Article in Human cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- A molecular landscape tracking the progression of non-muscle invasive bladder cancer.World journal of urology · 2026Review
- Inhibiting autophagy enhances anti-cancer properties of sulforaphane.Scientific reports · 2026Article
- METTL1-mediated m7G modification promotes colorectal cancer metastasis via stabilization of ICAM-1.Molecular and cellular biochemistry · 2025Article
- Red deer (Cervus elaphus L.) antler stem cell culture medium inhibits prostate cancer cells.Histochemistry and cell biology · 2025Article
- Mathurameha ameliorates cardiovascular complications in high-fat diet/low-dose streptozotocin-induced type 2 diabetic rats: insights from histological and proteomic analysis.Journal of molecular histology · 2024Article
- Receptors and Host Factors for Enterovirus Infection: Implications for Cancer Therapy.Cancers · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
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