ArticleScientific reports2015
GSK3β mediates the carcinogenic effect of HPV16 in cervical cancer.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cellular Retinoic Acid Binding Protein 2 (CRABP2), Up-regulated by HPV E6/E7, Leads to Aberrant Activation of the Integrin β1/FAK/ERK Signaling Pathway and Aggravates the Malignant Phenotypes of Cervical Cancer.Biochemical genetics · 2024Article
- Ubiquitination and deubiquitination in the regulation of NJournal of molecular medicine (Berlin, Germany) · 2024Review
- Research progress on m6A demethylase FTO and its role in gynecological tumors.Frontiers in oncology · 2024Review
- miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention.International journal of molecular sciences · 2022Review
- Dual targeting of GSK3B and HDACs reduces tumor growth and improves survival in an ovarian cancer mouse model.Gynecologic oncology · 2020Article
- β-Catenin: oncogenic role and therapeutic target in cervical cancer.Biological research · 2020Review
- Review
- The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism.Cell death discovery · 2018Article
- Wnt/β‑catenin pathway activation and silencing of the APC gene in HPV‑positive human cervical cancer‑derived cells.Molecular medicine reports · 2018Article
- WWOX inhibits the invasion of lung cancer cells by downregulating RUNX2.Cancer gene therapy · 2016Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is one of the most prevalent and fatal cancers among women and infection of the human papillomavirus (HPV) is the most important risk factor. This study investigated how HPV16 regulated GSK3β expression and function to promote cervical cancers. The expression of GSK3β was analyzed by quantitative PCR and western blot. The proliferation, invasion, and clonogenic survival of cells with different E6/E7 levels were measured by MTT, transwell invasion assays, and soft agar colony-forming assays, respectively. The levels of GSK3β were correlated with the copy numbers and expression levels of HPV16 E6/E7 genes. HPV16 E6/E7 genes regulated GSK3β transcription through an element located in the promoter 85 and 250 base pairs upstream of the transcription start site. The abilities of cell proliferation, invasion, and clonogenic survival were increased in C33A cells by ectopic HPV16 E6/E7 and decreased in CaSki cells by knocking down HPV16 E6/E7 levels. Meanwhile, LiCl increased GSK3β transcript levels and the proliferation of CaSki cells in a HPV16-dependent manner. These data indicated that GSK3β may participated in HPV16 mediated deregulation of wnt/β-catenin and other signaling pathways promoting the progression and invasion of cervical cancers.
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