Recognition and processing of cisplatin- and oxaliplatin-DNA adducts

Chaney, Stephen G.; Campbell, Sharon L.; Bassett, Ekaterina; Wu, Yibing

doi:10.1016/j.critrevonc.2004.08.008

Cited by 316 publications

(276 citation statements)

References 92 publications

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“…These results are consistent with those in the literature, including our previous work (Kiyota et al, 2002;Chaney et al, 2005), in which we reported that EGFR inhibitors are generally characterised by a cytostatic effect associated with enrichment of the G0/G1 phase of the cell cycle. Moreover, for each cell line, we showed that the effects on cell cycle of oxaliplatin/cetuximab together are additive of the effect of each molecule used alone.…”

Section: Discussionsupporting

confidence: 93%

“…In HCT-8 cells exposed to oxaliplatin/cetuximab, morphologic changes associated with apoptosis (DNA condensation and fragmentation) occurred 24 h earlier than in cells exposed to oxaliplatin alone and could play a role in the enhanced antiproliferative effects that we observed previously (Chaney et al, 2005). In HCT-8 cells, oxaliplatin exposure promoted survival through AKT activation; cetuximab exposure concomitant with oxaliplatin inhibited this regulation and induced restoration of apoptosis through the inhibition of oxaliplatin-induced AKT activation.…”

Section: Discussionmentioning

confidence: 49%

“…Nucleotide excision repair is the main DNA repair mechanism involved in oxaliplatin -DNA adduct repair (Reed, 1998;Chaney et al, 2005). This mechanism is associated with adduct recognition proteins such as XPA and XPC (xeroderma pigmentosum A and C: DNA-lesion recognition proteins) and with proteins such as ERCC1, which catalyses excision of the damaged nucleotide.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, platinum complexes are very reactive with the cysteine residue of glutathione (GSH), which detoxifies these compounds by a rapid binding mechanism. The nucleotide excision repair (NER) is the main cellular process involved in the elimination of oxaliplatin -DNA platinum adducts (Chaney et al, 2005) where excision repair cross complementation group1 (ERCC1) is the key enzyme leading to the 5 0 incision of the platinum DNA damage (Reed, 1998). Excision repair cross complementation group1 exists as mRNA and as protein in at least two forms.…”

mentioning

confidence: 99%

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Cetuximab potentiates oxaliplatin cytotoxic effect through a defect in NER and DNA replication initiation

Balin-Gauthier

Delord

et al. 2008

Br J Cancer

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Preclinical studies have demonstrated that the chemotherapeutic action of oxaliplatin, a third generation platinum derivative, is improved when combined with cetuximab, a monoclonal antibody inhibitor of epidermal growth factor receptors. To explore the mechanism of this synergistic benefit, we used HCT-8 and HCT-116, two human colon cancer cell lines, respectively, responsive and non-responsive to the oxaliplatin/cetuximab combination. We examined the effect of drug exposure on glutathione-S-transferasemediated oxaliplatin detoxification, DNA -platinum adducts formation, cell cycle distribution, apoptosis, and the expression of multiple targets involved in DNA replication, recombination, and repair. The major changes we found in HCT-8 were a stimulation of oxaliplatin -DNA adduct formation associated with reduced expression of the key enzyme (excision repair cross complementation group1: ERCC1) in the key repair process of oxaliplatin -DNA platinum adduct, the nucleotide excision repair (NER), both at the mRNA and protein levels. We also observed a reduced expression of factors involved in DNA replication initiation, which correlates with an enrichment of cells in the G1 phase of the cell cycle as well as an acceleration of apoptosis. None of these changes occurred in the non-responsive HCT-116 cell that we used as a negative control. These findings support the fact that cetuximab potentiates the oxaliplatin-mediated cytotoxic effect as the result of inhibition of NER and also DNA replication initiation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Cetuximab potentiates oxaliplatin cytotoxic effect through a defect in NER and DNA replication initiation

Balin-Gauthier

Delord

et al. 2008

Br J Cancer

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“…A decrease in mismatch repair has also been previously associated with cisplatin resistance, as the binding of the mismatch repair complex to Pt-DNA adducts appears to increase the cytotoxicity of the adducts, either by activating apoptosis or by causing "futile cycling" during trans-lesion synthesis past Pt-DNA adducts [27]. Mismatch repair protein MSH2 was examined by Western blot and real time PCR and found not to have changed in the resistant cell lines (data not shown).…”

Section: No Change In Dna Repair Capacity Associated With Platinum Rementioning

confidence: 83%

ERCC1 expression and RAD51B activity correlate with cell cycle response to platinum drug treatment not DNA repair

Stordal

Davey

2008

Cancer Chemother Pharmacol

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Metallodrugs: an approach against invasion and metastasis in cancer treatment

2022

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Cancer is a heterogeneous and multifactorial disease that causes high mortality throughout the world; therefore, finding the most effective therapies is a major research challenge. Currently, most anticancer drugs present a limited number of well‐established targets, such as cell proliferation or death; however, it is important to consider that the worse progression of cancer toward pathological stages implies invasion and metastasis processes. Medicinal Inorganic Chemistry (MIC) is a young area that deals with the design, synthesis, characterization, preclinical evaluation, and mechanism of action of new inorganic compounds, called metallodrugs. The properties of metallic ions allow enriching of strategies for the design of new drugs, enabling the adjustment of physicochemical and stereochemical properties. Metallodrugs can adopt geometries, such as tetrahedral, octahedral, square planar, and square planar pyramid, which adjusts their arrangement and facilitates binding with a wide variety of targets. The redox properties of some metal ions can be modulated by the presence of the bound ligands to adjust their interaction, thereby opening a range of mechanisms of action. In this regard, the mechanisms of action that trigger the biological activity of metallodrugs have been generally identified by: (a) coordination of the metal to biomolecules (for instance, cisplatin binds to the N7 in DNA guanine, as Pt‐N via coordination of the inhibition of enzymes); (b) redox‐active; and (c) ROS production. For this reason, a series of metallodrugs can interact with several specific targets in the anti‐invasive processes of cancer and can prevent metastasis. The structural base of several metal compounds shows great anticancer potential by inhibiting the signaling pathways related to cancer progression. In this minireview, we present the advances in the field of antimetastatic effects of metallodrugs.

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Recognition and processing of cisplatin- and oxaliplatin-DNA adducts

Cited by 316 publications

References 92 publications

Cetuximab potentiates oxaliplatin cytotoxic effect through a defect in NER and DNA replication initiation

Cetuximab potentiates oxaliplatin cytotoxic effect through a defect in NER and DNA replication initiation

ERCC1 expression and RAD51B activity correlate with cell cycle response to platinum drug treatment not DNA repair

Metallodrugs: an approach against invasion and metastasis in cancer treatment

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