ArticleGene therapy2013
Ruthenium oligonucleotides, targeting HPV16 E6 oncogene, inhibit the growth of cervical cancer cells under illumination by a mechanism involving p53.
Article in Gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Nucleic Acid Therapeutics for "Undruggable" Cancer Targets: Mechanisms, Challenges, and Prospects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Silencing HPV: the rise of RNA therapeutics in cervical cancer.Infectious agents and cancer · 2026Review
- Review
- Human papillomavirus infection, cervical cancer and the less explored role of trace elements.Biological trace element research · 2023Review
- Article
- Targeted Gene Delivery Therapies for Cervical Cancer.Cancers · 2020Review
- Human Papillomavirus E6 and E7: The Cervical Cancer Hallmarks and Targets for Therapy.Frontiers in microbiology · 2019Review
- Applications of Ruthenium Complexes Covalently Linked to Nucleic Acid Derivatives.Molecules (Basel, Switzerland) · 2018Review
- Synthesis and photophysical studies of a multivalent photoreactive RuBeilstein journal of organic chemistry · 2018Article
- Photochemically active DNA-intercalating ruthenium and related complexes - insights by combining crystallography and transient spectroscopy.Chemical science · 2017Article
- A novel intracellular antibody against the E6 oncoprotein impairs growth of human papillomavirus 16-positive tumor cells in mouse models.Oncotarget · 2016Article
- Combination of Ru(ii) complexes and light: new frontiers in cancer therapy.Chemical science · 2015Article
- Nip the HPV encoded evil in the cancer bud: HPV reshapes TRAILs and signaling landscapes.Cancer cell international · 2013Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk Human Papillomaviruses (HPV) has been found to be associated with carcinomas of the cervix, penis, vulva/vagina, anus, mouth and oro-pharynx. As the main tumorigenic effects of the HPV have been attributed to the expression of E6 and E7 genes, different gene therapy approaches have been directed to block their expression such as antisense oligonucleotides (ASO), ribozymes and small interfering RNAs. In order to develop a gene-specific therapy for HPV-related cancers, we investigated a potential therapeutic strategy of gene silencing activated under illumination. Our aim according to this antisense therapy consisted in regulating the HPV16 E6 oncogene by using an E6-ASO derivatized with a polyazaaromatic ruthenium (Ru(II)) complex (E6-Ru-ASO) able, under visible illumination, to crosslink irreversibly the targeted sequence. We examined the effects of E6-Ru-ASO on the expression of E6 and on the cell growth of cervical cancer cells. We demonstrated using HPV16(+) SiHa cervical cancer cells that E6-Ru-ASO induces after illumination, a reactivation of p53, the most important target of E6, as well as the inhibition of cell proliferation with a selective repression of E6 at the protein level. These results suggest that E6-Ru ASOs, activated under illumination and specifically targeting E6, are capable of inhibiting HPV16(+) cervical cancer cell proliferation.
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