ArticleInternational journal of oncology2018
Upregulation of E‑cadherin expression mediated by a novel dsRNA suppresses the growth and metastasis of bladder cancer cells by inhibiting β-catenin/TCF target genes.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Small Activating RNAs: A Curated Database and an Overview of Rational Design Principles.Molecules (Basel, Switzerland) · 2026Review
- Effect of smoking on the recurrence and progression of non-muscle-invasive bladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Nucleic acid drugs: recent progress and future perspectives.Signal transduction and targeted therapy · 2024Review
- Modulating the expression of tumor suppressor genes using activating oligonucleotide technologies as a therapeutic approach in cancer.Molecular therapy. Nucleic acids · 2023Review
- Nuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea.Experimental biology and medicine (Maywood, N.J.) · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low expression levels of E‑cadherin are correlated with poor prognosis in patients with bladder cancer (BCa). A small activating RNA (saRNA) targeting a specific promoter region can activate gene expression. In the present study, two small double-stranded RNAs (dsRNAs) targeting the promoter region of human E‑cadherin were designed and synthesized, and the regulatory role of saRNAs in E‑cadherin expression was investigated. The results of reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that transfection of dsEcad‑346 into the BCa cell lines T24 and 5637 significantly activated E‑cadherin expression. Furthermore, transfection of dsEcad‑346 and miR‑373 induced cell cycle arrest in G0/G1 phase, promoted apoptosis and significantly inhibited migration and invasion of BCa cells. Results of immunofluorescence and western blotting indicated that β-catenin was redistributed from the nucleus to the cell membrane following transfection of dsEcad‑346 and miR‑373. Additionally, the expression of β-catenin/T-cell factor complex (TCF) target genes (c‑MYC, matrix metallopeptidase 2, cyclin D1) was suppressed following transfection of BCa cells with saRNA. Silencing of E‑cadherin expression blocked the inhibitory effect of dsEcad‑346 and miR‑373 on BCa cells. In conclusion, a novel designed dsEcad‑346 can activate the expression of E‑cadherin in BCa cells. saRNA-mediated activation of E‑cadherin expression inhibited the growth and metastasis of BCa cells by promoting the redistribution of β-catenin from nucleus to cell membrane and inhibiting the β-catenin/TCF target genes.
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Registered trials
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