ArticleNucleic acids research2006
Tumor inhibition by genomically integrated inducible RNAi-cassettes.
Article in Nucleic acids research, 2006. 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, 32 citations in OpenAlex.
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- Embedding siRNA sequences targeting apolipoprotein B100 in shRNA and miRNA scaffolds results in differential processing and in vivo efficacy.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Conditional gene manipulation: Cre-ating a new biological era.Journal of Zhejiang University. Science. B · 2012Review
- Cdk1/cyclin B1 controls Fas-mediated apoptosis by regulating caspase-8 activity.Molecular and cellular biology · 2010Article
- Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy.Nature reviews. Drug discovery · 2010Review
- RNAi reduces expression and intracellular retention of mutant cartilage oligomeric matrix protein.PloS one · 2010Article
- In vivo gene regulation using tetracycline-regulatable systems.Advanced drug delivery reviews · 2009Review
- A novel short hairpin RNA (shRNA) expression system promotes Sox9-dependent gene silencing.Plasmid · 2009Article
- RNA interference: from basic research to therapeutic applications.Angewandte Chemie (International ed. in English) · 2009Review
- Contemporary approaches for modifying the mouse genome.Physiological genomics · 2008Review
- Development and implementation of a miniaturized high-throughput time-resolved fluorescence energy transfer assay to identify small molecule inhibitors of polo-like kinase 1.Assay and drug development technologies · 2007Article
- Reversible gene knockdown in mice using a tight, inducible shRNA expression system.Nucleic acids research · 2007Article
- Comparison of RNAi efficiency mediated by tetracycline-responsive H1 and U6 promoter variants in mammalian cell lines.Nucleic acids research · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA interference (RNAi) has emerged as a powerful tool to induce loss-of-function phenotypes by post-transcriptional silencing of gene expression. In this study we wondered whether inducible RNAi-cassettes integrated into cellular DNA possess the power to trigger neoplastic growth. For this purpose inducible RNAi vectors containing tetracycline (Tet)-responsive derivatives of the H1 promoter for the conditional expression of short hairpin RNA (shRNA) were used to target human polo-like kinase 1 (Plk1), which is overexpressed in a broad spectrum of human tumors. In the absence of doxycycline (Dox) HeLa clones expressing TetR, that carry the RNAi-cassette stably integrated, exhibited no significant alteration in Plk1 expression levels. In contrast, exposure to Dox led to marked downregulation of Plk1 mRNA to 3% and Plk1 protein to 14% in cell culture compared to mismatch shRNA/Plk1-expressing cells. As a result of Plk1 depletion cell proliferation decreased to 17%. Furthermore, for harnessing RNAi for silencing disease-related genes in vivo we transplanted inducible RNAi-HeLa cells onto nude mice. After administration of Dox knockdown of Plk1 expression was observed correlating to a significant inhibition of tumor growth. Taken together, our data revealed that genomically integrated RNAi-elements are suitable to hamper tumor growth by conditional expression of shRNA.
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