Gene-specific formation and repair of cisplatin intrastrand adducts and interstrand cross-links in Chinese hamster ovary cells.

Jones, Jennifer; Zhen, Weiping; Reed, Eddie; Parker, Ricardo J.; Sancar, Aziz; Bohr, Vilhelm A.

doi:10.1016/s0021-9258(20)89616-1

Cited by 140 publications

(23 citation statements)

References 30 publications

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“…Our data do not provide exact information on the density of cisplatin-induced DNA lesions during the CldU labeling period. However, previous atomic absorption studies showed that treatment with 300 mM cisplatin for 60 min lead to 1.65 adducts/10 Kb in Chinese hamster ovary cells (Jones et al, 1991). Based on this published data, we could estimate that the number of cisplatin-induced DNA lesions when using 150 mM cisplatin for 60 min is approximately 1 adduct every 12 Kb.…”

Section: Dna Fiber Assaymentioning

confidence: 76%

PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells

et al. 2020

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Summary Acute treatment with replication-stalling chemotherapeutics causes reversal of replication forks. BRCA proteins protect reversed forks from nucleolytic degradation, and their loss leads to chemosensitivity. Here, we show that fork degradation is no longer detectable in BRCA1-deficient cancer cells exposed to multiple cisplatin doses, mimicking a clinical treatment regimen. This effect depends on increased expression and chromatin loading of PRIMPOL and is regulated by ATR activity. Electron microscopy and single-molecule DNA fiber analyses reveal that PRIMPOL rescues fork degradation by reinitiating DNA synthesis past DNA lesions. PRIMPOL repriming leads to accumulation of ssDNA gaps while suppressing fork reversal. We propose that cells adapt to repeated cisplatin doses by activating PRIMPOL repriming under conditions that would otherwise promote pathological reversed fork degradation. This effect is generalizable to other conditions of impaired fork reversal (e.g., SMARCAL1 loss or PARP inhibition) and suggests a new strategy to modulate cisplatin chemosensitivity by targeting the PRIMPOL pathway.

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Section: Dna Fiber Assaymentioning

confidence: 76%

PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells

et al. 2020

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“…It is believed that the anticancer activity of Pt(II) based drugs such as cis -DDP ( cis- [Pt(NH 3 ) 2 Cl 2 ]) is due to the formation of one or more bifunctional adducts. − The most frequent adducts are intrastrand d(GpG) and d(ApG), − and there is substantial evidence that one or both of them may be responsible for the anticancer activity. ,− However, there is also evidence implicating the lower frequency GG interstrand adducts. − We have designed a series of complexes to interact stereospecifically with DNA and so give rise to an adduct profile different from that formed by cis -DDP. − The long-term aim of these studies is to investigate any correlation between anticancer activity and adduct profile and so contribute to an understanding of the mechanism of action of Pt anticancer drugs.…”

Section: Introductionmentioning

confidence: 99%

“…3,[9][10][11][12][13] However, there is also evidence implicating the lower frequency GG interstrand adducts. [14][15][16] We have designed a series of complexes to interact stereospecifically with DNA and so give rise to an adduct profile different from that formed by cis-DDP. [17][18][19][20][21] The long-term aim of these studies is to investigate any correlation between anticancer activity and adduct profile and so contribute to an understanding of the mechanism of action of Pt anticancer drugs.…”

Section: Introductionmentioning

confidence: 99%

Combined NMR and Molecular Mechanics Study of the Isomers Formed in the Reaction of Dichloro(1,4-diazacycloheptane)platinum(II) with the Dinucleotide d(GpG)

1996

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The reaction of [Pt(hpip)Cl 2 ] (hpip ) homopiperazine ) 1,4-diazacycloheptane) with d(GpG) yields two apparently isomeric products, separable by HPLC. These have been characterized by a combination of 2D NMR and molecular mechanics modeling. NOESY correlations between the H8 protons show that both products are head-to-head isomers, and NOESY correlations between the d(GpG) dinucleotide and the diamine ligand show that the difference between the isomers lies in the orientation of the two and three carbon chains of the hpip ligand with respect to the heads (H8 protons) of the guanine bases. Molecular mechanics calculations yield total energies that are consistent with the observation of the two isomers in approximately equal amounts.

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“…Analogously to the repair of u.v.-DNA adducts, cells probably manage cisplatin-DNA adducts in the same way. It has also been shown that the removal of the major cisplatin adducts involves nucleotide excision repair in bacterial [10-12] and mammalian cells [13,14]. These results suggest that the repair process of the cisplatin adduct is probably the same, at least in part, as that of ' u.v.-type' excision repair.…”

Section: Introductionmentioning

confidence: 95%

Characterization of a DNA-damage-recognition protein from F9 teratocarcinoma cells, which is inducible by retinoic acid and cyclic AMP

Chao

Sun

Lin‐Chao

1993

Biochemical Journal

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A nuclear protein that recognizes u.v.-damaged DNA was detected in extracts from murine F9 embryonic stem cells using a DNA-binding assay. The nuclear-protein-binding activity was increased in cells after treatment with retinoic acid/dibutyryl cyclic AMP (dbcAMP), with optimum induction at 6 days. In vitro treatment of nuclear extracts with agents that affect protein conformation (such as urea, Nonidet P40 and Ca2+) slightly modulated the damage-recognition activity. Furthermore, treatment of nuclear extracts with phosphatase dramatically inhibited the binding activity. In addition, damaged-DNA recognition of the nuclear extracts was effectively inhibited by damaged double- and single-stranded DNA. The expression of the nuclear protein with similar characteristics was abundant in HeLa cells and was increased in drug- or u.v.-resistant cells. The findings suggest that the recognition of a u.v.-DNA adduct is modulated, at least in part, by an activity that is induced during retinoic acid/dbcAMP-induced differentiation. These results also imply that the identified damage-recognition protein may be important for the sensitivity or resistance of mammalian cells to DNA damage.

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Gene-specific formation and repair of cisplatin intrastrand adducts and interstrand cross-links in Chinese hamster ovary cells.

Cited by 140 publications

References 30 publications

PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells

PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells

Combined NMR and Molecular Mechanics Study of the Isomers Formed in the Reaction of Dichloro(1,4-diazacycloheptane)platinum(II) with the Dinucleotide d(GpG)

Characterization of a DNA-damage-recognition protein from F9 teratocarcinoma cells, which is inducible by retinoic acid and cyclic AMP

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