ArticleBMC cancer2010
Decreased transcription-coupled nucleotide excision repair capacity is associated with increased p53- and MLH1-independent apoptosis in response to cisplatin.
Article in BMC cancer, 2010. 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, 37 citations in OpenAlex.
- Review
- The ubiquitin ligase UBR4 and the deubiquitylase USP5 modulate the stability of DNA mismatch repair protein MLH1.The Journal of biological chemistry · 2024Article
- CUL4A silencing attenuates cervical carcinogenesis and improves Cisplatin sensitivity.Molecular and cellular biochemistry · 2024Article
- The Role of Extracellular Vesicles in Mediating Resistance to Anticancer Therapies.International journal of molecular sciences · 2021Review
- Review
- Adipose most abundant 2 protein is a predictive marker for cisplatin sensitivity in cancers.Scientific reports · 2021Observational
- A Nobel-Winning Scientist: Aziz Sancar and the Impact of his Work on the Molecular Pathology of Neoplastic Diseases.Turk patoloji dergisi · 2021Review
- Role of Nucleotide Excision Repair in Cisplatin Resistance.International journal of molecular sciences · 2020Review
- CSB affected on the sensitivity of lung cancer cells to platinum-based drugs through the global decrease of let-7 and miR-29.BMC cancer · 2019Article
- Review
- Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019Article
- Loss of CUL4A expression is underlying cisplatin hypersensitivity in colorectal carcinoma cells with acquired trabectedin resistance.British journal of cancer · 2017Article
- Nucleotide excision repair deficiency increases levels of acrolein-derived cyclic DNA adduct and sensitizes cells to apoptosis induced by docosahexaenoic acid and acrolein.Mutation research · 2016Article
- The CSB repair factor is overexpressed in cancer cells, increases apoptotic resistance, and promotes tumor growth.DNA repair · 2013Article
- Article
- Expression of the mismatch repair gene hMLH1 is enhanced in non-small cell lung cancer with EGFR mutations.PloS one · 2013Article
- Alterations in nuclear pore architecture allow cancer cell entry into or exit from drug-resistant dormancy.The American journal of pathology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOne of the most commonly used classes of anti-cancer drugs presently in clinical practice is the platinum-based drugs, including cisplatin. The efficacy of cisplatin therapy is often limited by the emergence of resistant tumours following treatment. Cisplatin resistance is multi-factorial but can be associated with increased DNA repair capacity, mutations in p53 or loss of DNA mismatch repair capacity.
methodsRNA interference (RNAi) was used to reduce the transcription-coupled nucleotide excision repair (TC-NER) capacity of several prostate and colorectal carcinoma cell lines with specific defects in p53 and/or DNA mismatch repair. The effect of small inhibitory RNAs designed to target the CSB (Cockayne syndrome group B) transcript on TC-NER and the sensitivity of cells to cisplatin-induced apoptosis was determined.
resultsThese prostate and colon cancer cell lines were initially TC-NER proficient and RNAi against CSB significantly reduced their DNA repair capacity. Decreased TC-NER capacity was associated with an increase in the sensitivity of tumour cells to cisplatin-induced apoptosis, even in p53 null and DNA mismatch repair-deficient cell lines.
conclusionThe present work indicates that CSB and TC-NER play a prominent role in determining the sensitivity of tumour cells to cisplatin even in the absence of p53 and DNA mismatch repair. These results further suggest that CSB represents a potential target for cancer therapy that may be important to overcome resistance to cisplatin in the clinic.
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