ArticleOncology reports2017
Inhibitor of β-catenin and TCF (ICAT) promotes cervical cancer growth and metastasis by disrupting E-cadherin/β-catenin complex.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Feasibility of machine learning-based modeling and prediction to assess osteosarcoma outcomes.Scientific reports · 2025Article
- Multidimensional outlook on the pathophysiology of cervical cancer invasion and metastasis.Molecular and cellular biochemistry · 2023Review
- SNPs in 3'UTR miRNA Target Sequences Associated with Individual Drug Susceptibility.International journal of molecular sciences · 2022Review
- ICAT promotes colorectal cancer metastasis via binding to JUP and activating the NF-κB signaling pathway.Journal of clinical laboratory analysis · 2022Article
- Article
- Recent insights into the microRNA-dependent modulation of gliomas from pathogenesis to diagnosis and treatment.Cellular & molecular biology letters · 2022Review
- RNA-binding motif protein 10 represses tumor progression through the Wnt/β- catenin pathway in lung adenocarcinoma.International journal of biological sciences · 2022Article
- β-Catenin: oncogenic role and therapeutic target in cervical cancer.Biological research · 2020Review
- miR‑296‑3p promotes the proliferation of glioblastoma cells by targeting ICAT.Molecular medicine reports · 2020Article
- Functional genetic variants ofJournal of Cancer · 2020Article
- Cancer IgG, a potential prognostic marker, promotes colorectal cancer progression.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019Article
- Silencing of CARMA3 inhibits bladder cancer cell migration and invasion via deactivating β-catenin signaling pathway.OncoTargets and therapy · 2019Article
- Zeylenone represses the progress of human prostate cancer by downregulating the Wnt/β‑catenin pathway.Molecular medicine reports · 2018Article
- Long non-coding RNA linc01433 promotes migration and invasion in non-small cell lung cancer.Thoracic cancer · 2018Article
- Preoperative SCC-Ag and thrombocytosis as predictive markers for pelvic lymphatic metastasis of squamous cervical cancer in early FIGO stage.Journal of Cancer · 2018Article
- Overexpression of ICAT Inhibits the Progression of Colorectal Cancer by Binding with β-Catenin in the Cytoplasm.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitor of β-catenin and TCF (ICAT) blocks the binding of TCF to β-catenin and has been demonstrated as a suppressor of the Wnt/β-catenin signaling pathway. It has been reported to exert a different function around a wide variety of cancers. However, its function and underlying mechanisms in human cervical cancer remains unknown. In the present study, the expression of ICAT in 41 human cervical cancer tissues and 30 normal cervical tissues was evaluated by immunohistochemical analysis. ICAT was found highly expressed in cancer tissues. ICAT overexpression significantly promoted SiHa cell proliferation in vitro by causing G1 arrest, and enhanced cell migration and invasion whereas, ICAT knockdown induced opposite effects in Caski cells which have higher expression of ICAT. Downregulation or overexpression of ICAT resulted in an altered expression of the epithelial-mesenchymal transition (EMT). Furthermore, immunoprecipitation assays revealed that ICAT pormoted cervical cancer EMT by competing in E-cadhenin binding to β-caterin. Overexpression of ICAT in SiHa cells promoted tumor growth and EMT was also demonstrated by the xenograft mouse experiment. These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/β-catenin complex. It may be a novel potential therapeutic target for therapy in human cervical cancer.
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