Influence of treatment temperature on the genotoxic effects of cisplatin in CHO cells: cytotoxicity, mutagenicity and induction of lesions in DNA

Plooy, Adrie C.M.; Dijk, Margriet van; Berends, Frits J.; Lohman, P.H.M.

doi:10.1016/0027-5107(85)90191-5

Cited by 14 publications

(12 citation statements)

References 8 publications

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“…Because cisplatin DNA adducts are considered to be the main lesions that cause cellular death, the efficiency of removal of cisplatin by NER is expected to play an important role in drug response. Indeed, cells deficient in NER are hypersensitive to cisplatin [109,110] and several studies have shown a relationship between clinical resistance to cisplatin and increased level of NER proteins expression. Such correlation has been established in resistant ovarian, lung and gastric cancers for which the level of ERCC1, a NER protein which performs with XPF the 5' strand incision of the damaged strand was found to be increased [111][112][113].…”

Section: Cisplatin Sensitivity and Dna Repair Systemmentioning

confidence: 99%

Cisplatin Is a DNA-Damaging Antitumour Compound Triggering Multifactorial Biochemical Responses in Cancer Cells: Importance of Apoptotic Pathways

Sedletska¹,

Giraud-Panis²,

Malinge³

2005

CMCACA

181

126

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cis-diamminedichloroplatinum(II) (cisplatin) is among the most active antitumour agent used in human chemotherapy. The purpose of this review is to give an insight in several molecular mechanisms that mediate the sensitivity of cancer cells to this drug and to show how recent progress in our knowledge on some critical molecular events should lay the foundations of a more rational approach to anticancer drug design. Cisplatin is primarily considered as a DNA-damaging anticancer drug, mainly forming different types of bifunctional adducts in its reaction with cellular DNA. We will address the question of cellular activity disruption that cisplatin could cause through binding to more sensitive region of the genome such as telomeres. Cellular mechanisms of resistance to cisplatin are multifactorial and contribute to severe limitation in the use of this drug in clinics. They include molecular events modulating the amount of drug-DNA interaction, such as a reduction in cisplatin accumulation inside cancer cells or inactivation of cisplatin by thiol-containing species. Other important mechanisms acting downstream to the initial reaction of cisplatin with DNA, include an increase in adducts repair and a decrease in induction of apoptosis. Recently accumulating evidence suggest a role of the long patch DNA mismatch repair system in sensing cisplatin-damaged DNA and in triggering cell death through a c-Abl- and p73-dependent cascade; two other important pathways have been unravelled that are the mitogen-activated protein kinase cascade and the tumor suppressor p53. Several of these mechanisms underlying cisplatin resistance have been exploited to design new platinum derivatives. This issue will be covered in the present review.

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Section: Cisplatin Sensitivity and Dna Repair Systemmentioning

confidence: 99%

Cisplatin Is a DNA-Damaging Antitumour Compound Triggering Multifactorial Biochemical Responses in Cancer Cells: Importance of Apoptotic Pathways

Sedletska¹,

Giraud-Panis²,

Malinge³

2005

CMCACA

181

126

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“…Apart from transcription, cisplatin-DNA damage affects nucleotide excision repair (NER), an important pathway for removing the lesions 10,11. NER-defective human fibroblast cells derived from xeroderma pigmentosum (XP) patients are hypersensitive to platinum drugs 12. These cells contain specific defects in one of seven XP genes, XPA through XPG, and are generally more sensitive to treatment by platinum drugs compared to normal human fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Transcription Inhibition by Platinum−DNA Cross-Links in Live Mammalian Cells

2010

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We have investigated the processing of site-specific Pt-DNA cross-links in live mammalian cells to enhance our understanding of the mechanism of action of platinum-based anticancer drugs. The activity of platinum drugs against cancer is mediated by a combination of processes including cell entry, drug activation, DNA-binding, and transcription inhibition. These drugs bind nuclear DNA to form Pt-DNA cross-links, which arrest key cellular functions, including transcription, and trigger a variety of responses, such as repair. Mechanistic investigations into the processing of specific Pt-DNA cross-links are critical for understanding the effects of platinum DNA damage, but conventional in vitro techniques do not adequately account for the complex and intricate environment within a live cell. With this limitation in mind, we developed a strategy to study platinum cross-links on plasmid DNAs transfected into live mammalian cells based on luciferase reporter vectors containing defined platinum-DNA lesions that are either globally or site-specifically incorporated. Using cells with either competent or deficient nucleotide excision repair systems, we demonstrate that Pt-DNA cross-links impede transcription by blocking passage of the RNA polymerase complex and that nucleotide excision repair can remove the block and restore transcription. Results are presented for ~3800-base pair plasmids that are either globally platinated or carry a single 1,2-d(GpG) or 1,3-d(GpTpG) intrastrand cross-link formed by either cis-{Pt(NH3)2}2+ or cis-{Pt(R,R-dach)}2+; where {Pt(NH3)2}2+ is the platinum unit conveyed by cisplatin and carboplatin and R,R-dach is the oxaliplatin ligand, R,R-1,2-diaminocyclohexane.

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“…The significance of repair of DNA lesions for cellular tolerance to cis-DDP is demonstrated by studies of repair deficient baceria (13,14,15,16), yeast cells (17), Chinese hamster cells (18) and human xeroderma pigInentosum cells (19,20,21). It has been shown in vitro that the E. coli UvrABC nuclease incises the 8th phosphodiester bond 5' and the 4th phosphodiester bond 3' to GG intrastrand cross-links, thus excising an oligomer containing the adduct (16).…”

Section: Introductionmentioning

confidence: 99%

Repair synthesis by human cell extracts in DNA damaged bycis- andtrans-diamminedichloroplatinum(II)

Hansson¹,

Wood

1989

Nucl Acids Res

109

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DNA damage was induced in closed circular plasmid DNA by treatment with cis-or transdiamminedichloroplatinum(l). These plasmids were used as substrates in reactions to give quantitative measurements of DNA repair synthesis mediated by cell free extracts from human lymphoid cell lines. Adducts induced by both drugs stimulated repair synthesis in a dose dependent manner by an ATP-requiring process. Measurements by an isopycnic gradient sedimentation method gave an upper limit for the average patch sizes in this in vitro system of around 140 nucleotides. It was estimated that up to 3% of the drug adducts induce the synthesis of a repair patch. The repair synthesis is due to repair of a small fraction of frequent drug adducts, rather than extensive repair of a rare subclass of lesions. Nonspecific DNA synthesis in undamaged plasmids, caused by exonucleolytic degradation and resynthesis, was reduced by repeated purification of intact circular forms. An extract made from cells belonging to xeroderma pigmentosum complementation group A was deficient in repair synthesis in response to the presence of cis-or trans-diamminedichloroplatinum(ll) adducts in DNA.

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Influence of treatment temperature on the genotoxic effects of cisplatin in CHO cells: cytotoxicity, mutagenicity and induction of lesions in DNA

Cited by 14 publications

References 8 publications

Cisplatin Is a DNA-Damaging Antitumour Compound Triggering Multifactorial Biochemical Responses in Cancer Cells: Importance of Apoptotic Pathways

Cisplatin Is a DNA-Damaging Antitumour Compound Triggering Multifactorial Biochemical Responses in Cancer Cells: Importance of Apoptotic Pathways

Transcription Inhibition by Platinum−DNA Cross-Links in Live Mammalian Cells

Repair synthesis by human cell extracts in DNA damaged bycis- andtrans-diamminedichloroplatinum(II)

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