ArticleScientific reports2015
HPV16 early gene E5 specifically reduces miRNA-196a in cervical cancer cells.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Molecular interaction of human papilloma virus (HPV) with microRANs: insights into the development of cervical cancer and treatment approaches.Infectious agents and cancer · 2025Review
- Transcription factor c-Rel regulated by E5 affects the whole process after HPV16 infection through miR-133a-modulated feedback loop aim at mir-379-369 cluster.Cancer cell international · 2022Article
- Unravelling the Immunomodulatory Effects of Viral Ion Channels, towards the Treatment of Disease.Viruses · 2021Review
- Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021Review
- The Role of microRNAs, Long Non-coding RNAs, and Circular RNAs in Cervical Cancer.Frontiers in oncology · 2020Review
- High-Risk HPV Oncoproteins and PD-1/PD-L1 Interplay in Human Cervical Cancer: Recent Evidence and Future Directions.Frontiers in oncology · 2020Review
- Mucosal and Cutaneous Human Papillomavirus Infections and Cancer Biology.Frontiers in oncology · 2019Review
- Dysregulation of miR-375/AEG-1 Axis by Human Papillomavirus 16/18-E6/E7 Promotes Cellular Proliferation, Migration, and Invasion in Cervical Cancer.Frontiers in oncology · 2019Article
- S100A6 promotes the proliferation and migration of cervical cancer cells via the PI3K/Akt signaling pathway.Oncology letters · 2018Article
- HPV epigenetic mechanisms related to Oropharyngeal and Cervix cancers.Cancer biology & therapy · 2018Review
- Human Papillomavirus 16 Oncoproteins Downregulate the Expression of miR-148a-3p, miR-190a-5p, and miR-199b-5p in Cervical Cancer.BioMed research international · 2018Article
- A novel HPV16 E7-affitoxin for targeted therapy of HPV16-induced human cervical cancer.Theranostics · 2018Article
- Overexpression of microRNA-132 enhances the radiosensitivity of cervical cancer cells by down-regulating Bmi-1.Oncotarget · 2017Article
- Prevalence of Human Papilloma Virus in Sinonasal Papilloma in Southern Iranian Population.Journal of dentistry (Shiraz, Iran) · 2017Article
- miR-126-5p Restoration Promotes Cell Apoptosis in Cervical Cancer by Targeting Bcl2l2.Oncology research · 2017Article
- Use of Mature miRNA Strand Selection in miRNAs Families in Cervical Cancer Development.International journal of molecular sciences · 2017Review
- HPV disease transmission protection and control.Microbial cell (Graz, Austria) · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk human papillomavirus (HPV) type 16, which is responsible for greater than 50% of cervical cancer cases, is the most prevalent and lethal HPV type. However, the molecular mechanisms of cervical carcinogenesis remain elusive, particularly the early steps of HPV infection that may transform normal cervical epithelium into a pre-neoplastic state. Here, we report that a group of microRNAs (microRNAs) were aberrantly decreased in HPV16-positive normal cervical tissues, and these groups of microRNAs are further reduced in cervical carcinoma. Among these miRNAs, miR196a expression is the most reduced in HPV16-infected tissues. Interestingly, miR196a expression is low in HPV16-positive cervical cancer cell lines but high in HPV16-negative cervical cancer cell lines. Furthermore, we found that only HPV16 early gene E5 specifically down-regulated miRNA196a in the cervical cancer cell lines. In addition, HoxB8, a known miR196a target gene, is up-regulated in the HPV16 cervical carcinoma cell line but not in HPV18 cervical cancer cell lines. Various doses of miR196a affected cervical cancer cell proliferation and apoptosis. Altogether, these results suggested that HPV16 E5 specifically down-regulates miR196a upon infection of the human cervix and initiates the transformation of normal cervix cells to cervical carcinoma.
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