ArticleCellular oncology (Dordrecht, Netherlands)2020
WNT1, a target of miR-34a, promotes cervical squamous cell carcinoma proliferation and invasion by induction of an E-P cadherin switch via the WNT/β-catenin pathway.
Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- MicroRNA-Based Triage of HPV-Positive Women Using Liquid-Based Cytology: Diagnostic Performance and Network-Level Insights.Cancers · 2026Article
- The role of microRNAs in modulating Wnt signaling pathway dynamics and their therapeutic implications in non-small cell lung cancer.Discover oncology · 2026Review
- Gramine Suppresses Cervical Cancer by Targeting CDK2: Integrated Omics-Pharmacology and In Vitro Evidence.Current issues in molecular biology · 2026Article
- Novel Avenues for the Detection of Cancer-Associated Viral Genome Integrations Using Long-Read Sequencing Technologies.Cancers · 2025Review
- CouldBiomedicines · 2025Article
- Clinical value of miR-216a-5p and miR-34a in early screening for cervical cancer.American journal of translational research · 2025Article
- miRNAs Dysregulated in Human Papillomavirus-Associated Benign Prostatic Lesions and Prostate Cancer.Cancers · 2024Article
- Role of STAT3 in cancer cell epithelial‑mesenchymal transition (Review).International journal of oncology · 2024Review
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- 3D Chromatin Architecture Re-Wiring at theBiology · 2023Article
- Infection by High-Risk Human Papillomaviruses, Epithelial-to-Mesenchymal Transition and Squamous Pre-Malignant or Malignant Lesions of the Uterine Cervix: A Series of Chained Events?International journal of molecular sciences · 2021Review
- Long non-coding RNA-H19 promotes ovarian cancer cell proliferation and migration via the microRNA-140/Wnt1 axis.The Kaohsiung journal of medical sciences · 2021Article
- The microRNA miR-19a-3p suppresses cell growth, migration, and invasion in multiple myeloma via the Wnt/β-catenin pathway.Translational cancer research · 2021Article
- Cervical Cancer, Papillomavirus, and miRNA Dysfunction.Frontiers in molecular biosciences · 2021Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
purposePersistent infection with high-risk human papillomavirus (HR-HPV) is thought to play a prominent role in the initiation and progression of almost all cases of cervical cancer. Previously, we and others found that microRNA 34a (miR-34a) may be regulated by HR-HPV E6 to contribute to the development of cervical cancer. Here, we aimed to identify the oncogenic potential and clinical significance of a known miR-34a target, WNT1, in cervical squamous cell carcinoma (SCC) development and to investigate the associated mechanisms underlying cervical SCC cell proliferation and invasion.
methodsWNT1 and miR-34a expression levels were assessed in primary cervical lesions using immunohistochemistry and qRT-PCR, respectively. The cellular effects and the expression of its associated genes were examined in cervical SCC-derived Siha and Caski cells after siRNA-WNT1 (downregulation) or miR-34a mimic (upregulation) treatment. A cervical SCC xenograft mouse model was used to investigate the in vivo effects of miR-34a overexpression. HPV-16 E6/E7 expression was inhibited by gene promoter siRNA targeting, after which the levels of miR-34a and WNT1 were examined.
resultsWNT1 protein upregulation was found to be associated with a poor prognosis in cervical SCC patients. In vitro assays in Siha and Caski cells revealed that WNT1 downregulation decreased cell proliferation and invasion, inhibited WNT/β-catenin activation and affected the expression of E-cadherin and P-cadherin. MiR-34a upregulation resulted in decreased WNT1 expression. An inverse correlation between miR-34a and WNT1 expression was also observed in primary cervical SCC tissues. In addition, we found that MiR-34a could regulate an E-cadherin to P-cadherin switch (E-P cadherin switch) to inhibit cell proliferation and tumorigenesis in vitro and in vivo via inactivation of the WNT1/β-catenin pathway. Finally, we found that decreased HPV-16 E6/E7 expression resulted in miR-34a upregulation and WNT1 downregulation in Siha and Caski cells.
conclusionsFrom our results we conclude that WNT1, as a target of miR-34a, can promote cervical SCC cell proliferation and invasion by induction of an E-P cadherin switch via the WNT1/β-catenin pathway. Our results may provide new options for the treatment of patients with cervical SCC.
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