ArticleProceedings of the National Academy of Sciences of the United States of America2005
Genetic reprogramming of tumor cells by zinc finger transcription factors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Tumors hijack immune-privileging regulons via distinct cell types to confer T cell desertion and immunotherapy resistance across various cancers.Nature communications · 2026Article
- NFATC2 target gene signature correlates with immune checkpoint blockade resistance in melanoma.American journal of cancer research · 2025Article
- Epigenome engineering: new technologies for precision medicine.Nucleic acids research · 2020Article
- Reprogramming cell fate with artificial transcription factors.FEBS letters · 2018Review
- Randomized CRISPR-Cas Transcriptional Perturbation Screening Reveals Protective Genes against Alpha-Synuclein Toxicity.Molecular cell · 2017Article
- The pan-cancer pathological regulatory landscape.Scientific reports · 2016Article
- Genome-Editing Technologies: Principles and Applications.Cold Spring Harbor perspectives in biology · 2016Review
- Enhanced MyoD-induced transdifferentiation to a myogenic lineage by fusion to a potent transactivation domain.ACS synthetic biology · 2015Article
- Controlling gene networks and cell fate with precision-targeted DNA-binding proteins and small-molecule-based genome readers.The Biochemical journal · 2014Review
- Synthetic zinc finger proteins: the advent of targeted gene regulation and genome modification technologies.Accounts of chemical research · 2014Article
- Targeting serous epithelial ovarian cancer with designer zinc finger transcription factors.The Journal of biological chemistry · 2012Article
- Article
- Targeted silencing of the oncogenic transcription factor SOX2 in breast cancer.Nucleic acids research · 2012Article
- Chimeric piggyBac transposases for genomic targeting in human cells.Nucleic acids research · 2012Article
- Induction of stable drug resistance in human breast cancer cells using a combinatorial zinc finger transcription factor library.PloS one · 2011Article
- Modular system for the construction of zinc-finger libraries and proteins.Nature protocols · 2010Article
- Tra1 as a screening target for transcriptional activation domain discovery.Bioorganic & medicinal chemistry letters · 2009Article
- Systematic identification of transcription factors associated with patient survival in cancers.BMC genomics · 2009Article
- Oligomerized pool engineering (OPEN): an 'open-source' protocol for making customized zinc-finger arrays.Nature protocols · 2009Article
- Targeting the absence: homozygous DNA deletions as immutable signposts for cancer therapy.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Cancer arises by the accumulation of genetic alterations in DNA leading to aberrant gene transcription. Expression-profiling studies have correlated genomewide expression signatures with malignancy. However, functional analysis elucidating the contribution and synergy of genes in specific cancer cell phenotypes remains a formidable obstacle. Herein, we describe an alternative genetic approach for identification of genes involved in tumor progression by using a library of zinc finger artificial transcription factors (ATFs) and functional screening of tumor cells as a source of genetic plasticity and clonal selection. We isolated a six-zinc finger transcriptional activator (TF 20-VP, TF 20 containing the VP64 activator domain) that acts to reprogram a drug-sensitive, poorly invasive, and nonmetastatic cell line into a cell line with a drug-resistant, highly invasive, and metastatic phenotype. Differential expression profiles of cells expressing TF 20-VP followed by functional studies, both in vitro and in animal models, revealed that invasion and metastasis requires co-regulation of multiple target genes. Significantly, the E48 antigen, associated with poor metastasis-free survival in head and neck cancer, was identified as one specific target of TF 20-VP. We have shown phenotypic modulation of tumor cell behavior by E48 expression, including enhanced cell migration in vitro and tumor cell dissemination in vivo. This study demonstrates the use of ATFs to identify the group of genes that cooperate during tumor progression. By co-regulating multiple targets, ATFs can be used as master genetic switches to reprogram and modulate complex neoplastic phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.