ArticleBMC cancer2008
Knockdown of TFIIS by RNA silencing inhibits cancer cell proliferation and induces apoptosis.
Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- USP47-Mediated Deubiquitination and Stabilization of TCEA3 Attenuates Pyroptosis and Apoptosis of Colorectal Cancer Cells Induced by Chemotherapeutic Doxorubicin.Frontiers in pharmacology · 2021Article
- Elongation Factor TFIIS Prevents Transcription Stress and R-Loop Accumulation to Maintain Genome Stability.Molecular cell · 2019Article
- Transcription fidelity: New paradigms in epigenetic inheritance, genome instability and disease.DNA repair · 2019Review
- Novel Insights reveal Anti-microbial Gene Regulation of Piglet Intestine Immune in response to Clostridium perfringens Infection.Scientific reports · 2019Article
- TCEA1 regulates the proliferative potential of mouse myeloid cells.Experimental cell research · 2018Article
- Transformation-induced stress at telomeres is counteracted through changes in the telomeric proteome including SAMHD1.Life science alliance · 2018Article
- Accurate RNA consensus sequencing for high-fidelity detection of transcriptional mutagenesis-induced epimutations.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mechanism of DNA alkylation-induced transcriptional stalling, lesion bypass, and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Overexpression of EphB2 in hippocampus rescues impaired NMDA receptors trafficking and cognitive dysfunction in Alzheimer model.Cell death & disease · 2017Article
- Quantitative analysis of gene expression in fixed colorectal carcinoma samples as a method for biomarker validation.Molecular medicine reports · 2016Article
- TFIIS.h, a new target of p53, regulates transcription efficiency of pro-apoptotic bax gene.Scientific reports · 2016Article
- TCEA3 Attenuates Gastric Cancer Growth by Apoptosis Induction.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Visualizing translocation dynamics and nascent transcript errors in paused RNA polymerases in vivo.Genome biology · 2015Article
- Direct assessment of transcription fidelity by high-resolution RNA sequencing.Nucleic acids research · 2013Article
- Dysregulation of the basal RNA polymerase transcription apparatus in cancer.Nature reviews. Cancer · 2013Review
- RNF20 inhibits TFIIS-facilitated transcriptional elongation to suppress pro-oncogenic gene expression.Molecular cell · 2011Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundA common element among cancer cells is the presence of improperly controlled transcription. In these cells, the degree of specific activation of some genes is abnormal, and altering the aberrant transcription may therefore directly target cancer. TFIIS is a transcription elongation factor, which directly binds the transcription motor, RNA Polymerase II and allows it to read through various transcription arrest sites. We report on RNA interference of TFIIS, a transcription elongation factor, and its affect on proliferation of cancer cells in culture.
methodsRNA interference was performed by transfecting siRNA to specifically knock down TFIIS expression in MCF7, MCF10A, PL45 and A549 cells. Levels of TFIIS expression were determined by the Quantigene method, and relative protein levels of TFIIS, c-myc and p53 were determined by C-ELISA. Induction of apoptosis was determined by an enzymatic Caspase 3/7 assay, as well as a non-enzymatic assay detecting cytoplasmic mono- and oligonucleosomes. A gene array analysis was conducted for effects of TFIIS siRNA on MCF7 and MCF10A cell lines.
resultsKnockdown of TFIIS reduced cancer cell proliferation in breast, lung and pancreatic cancer cell lines. More specifically, TFIIS knockdown in the MCF7 breast cancer cell line induced cancer cell death and increased c-myc and p53 expression whereas TFIIS knockdown in the non-cancerous breast cell line MCF10A was less affected. Differential effects of TFIIS knockdown in MCF7 and MCF10A cells included the estrogenic, c-myc and p53 pathways, as observed by C-ELISA and gene array, and were likely involved in MCF7 cell-death.
conclusionAlthough transcription is a fundamental process, targeting select core transcription factors may provide for a new and potent avenue for cancer therapeutics. In the present study, knockdown of TFIIS inhibited cancer cell proliferation, suggesting that TFIIS could be studied as a potential cancer target within the transcription machinery.
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