ArticleOncoTargets and therapy2018
Inhibition of MUC1-C entering nuclear suppresses MYC expression and attenuates malignant growth in esophageal squamous cell carcinoma.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- TMEM59L promotes neuroendocrine differentiation and enzalutamide resistance in prostate cancer by regulating MUC1/β-catenin/MYC axis.Clinical and translational medicine · 2026Article
- Establishment and validation of the prognostic risk model based on the anoikis-related genes in esophageal squamous cell carcinoma.Annals of medicine · 2024Article
- Interleukin 33 supports squamous cell carcinoma growth via a dual effect on tumour proliferation, migration and invasion, and T cell activation.Cancer immunology, immunotherapy : CII · 2024Article
- Targeting MUC1-C reverses the cisplatin resistance of esophageal squamous cell carcinomaTranslational cancer research · 2021Article
- Evodiamine suppresses non-small cell lung cancer by elevating CD8Journal of experimental & clinical cancer research : CR · 2020Article
- MUC1-C in chronic inflammation and carcinogenesis; emergence as a target for cancer treatment.Carcinogenesis · 2020Review
- Bioinformatics-based analysis of the lncRNA-miRNA-mRNA and TF regulatory networks reveals functional genes in esophageal squamous cell carcinoma.Bioscience reports · 2020Article
- MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer.Nature communications · 2020Article
- Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.Journal of cellular physiology · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mucin 1 (MUC1) heterodimeric protein (N-terminal subunit and C-terminal subunit) is aberrantly overexpressed in esophageal squamous cell carcinoma (ESCC) and has been linked to poor outcomes in this disease. The detailed mechanism(s), however, remains unclear. In this article, we investigate the effects of the MUC1 C-terminal transmembrane subunit (MUC1-C) through the inhibitor GO-201, which inhibits MUC1-C targeting to nuclear. PATIENTS AND
methodsThe expression of MUC1-C and MYC in the ESCC samples and cell lines was detected by immunohistochemistry, immunofluorescence and western blotting. MYC mRNA level was determined by using quantitative real-time polymerase chain reaction. In addition, Cell Counting Kit-8, clonogenic assay, transwell assay and tumor xenograft in nude mice assay were utilized to determine the role of MUC1-C in proliferation, invasion and migration of ESCC cells.
resultsThe level of MUC1-C in nuclear and MYC in whole cells in the ESCC tissue is significantly higher than that in the noncancerous tissue. Treatment of MUC1-C-overexpressing ESCC cells with GO-201 was associated with downregulation of MYC expression and induction of apoptosis. Besides, in vitro and in vivo assays have both shown that inhibiting MUC1-C targeting to the nucleus by the GO-201 significantly decreased the abilities of proliferation, invasion and migration in ESCC cells.
conclusionOur findings suggest that MUC1-C targeting to the nucleus plays an important role in suppressing the malignant growth of ESCC and indicate that MUC1-C is a potential target for the treatment of ESCC.
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