2008
DOI: 10.1007/s00280-008-0783-x
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ERCC1 expression and RAD51B activity correlate with cell cycle response to platinum drug treatment not DNA repair

Abstract: Background: The H69CIS200 and H69OX400 cell lines are novel models of low-

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Cited by 7 publications
(8 citation statements)
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“…Moreover, S-phase arrests (indicative of high DNA damage 16 ) were already detected at cisplatin doses of 5 mM for the GM04312 cells and 20 mM for the A2780 cells. For the A2780 cells at lower doses, and for the A549 and A2780cis cells at all cisplatin concentrations, the results revealed cell cycle arrests at the G2/M-phase, as described before for cisplatin treatments, 18 even after low dose exposure. 8 Considering that low levels of XPA protein were specifically related to cisplatin sensitivity 40 and to increased cell apoptosis, 41 the highest sensitivity of the GM04312 cells was most likely due to the lack of XPA protein.…”
Section: Discussionmentioning
confidence: 69%
See 1 more Smart Citation
“…Moreover, S-phase arrests (indicative of high DNA damage 16 ) were already detected at cisplatin doses of 5 mM for the GM04312 cells and 20 mM for the A2780 cells. For the A2780 cells at lower doses, and for the A549 and A2780cis cells at all cisplatin concentrations, the results revealed cell cycle arrests at the G2/M-phase, as described before for cisplatin treatments, 18 even after low dose exposure. 8 Considering that low levels of XPA protein were specifically related to cisplatin sensitivity 40 and to increased cell apoptosis, 41 the highest sensitivity of the GM04312 cells was most likely due to the lack of XPA protein.…”
Section: Discussionmentioning
confidence: 69%
“…[11][12][13][14][15] However, there are some inconsistencies in the literature regarding the value of the cisplatin-DNA adduct level per se as a resistance predictive factor. 8,12 It has been known for several years that cisplatin treatment is able to modify cell cycle progression, [16][17][18] and that this modification could be different for sensitive and resistant cells. 17 Furthermore, cisplatin can also induce genomic instability, which is generally measured as the presence of DNA strand breaks.…”
Section: Introductionmentioning
confidence: 99%
“…Thus, their siRNA-mediated gene silencing affects DNA repair efficiency negatively in oxaliplatin-treated cells making them more sensitive to the drug (39). Some negative studies also exist, such as that from Stordal and colleagues, who reported a decrease in ERCC1 in association with oxaliplatin-induced cell-cycle arrest but not with resistance or altered DNA repair capacity (40). Using an in vitro model of oxaliplatin-acquired resistance, we showed that parental cells were able to upregulate XPD (xeroderma pygmentosum group D, ERCC2) and ERCC1 gene expression, whereas oxaliplatin-resistant derived cells were not (11).…”
Section: The Glutathione Systemmentioning
confidence: 99%
“…There are at least two alternative explanations, either (1) HU treatment generated stalled replication forks during S phase of the cell cycle due to reduced HR-repair subsequent to RAD51B -knockdown as HU causes stalled replication forks by depleting the pool of certain nucleotides that are used to extend the replicating strands, or (2) RAD51B may directly influence the cell cycle by interacting with a component of the checkpoint response pathway, similar to the interaction observed between BRCA1 and cell cycle regulation proteins. 64 Based on the expression data under conditions that did not lead to significant differences in viability/proliferation, as well as a previous study on RAD51B protein foci formation in response to platinum drug treatment, 39 we believe it is highly likely for RAD51B to interfere with the cell cycle checkpoint independent of its role in HR repair. However, further work is needed to confirm this interpretation.…”
Section: Discussionmentioning
confidence: 77%
“… 38 In addition, RAD51B has been implicated in the cellular response to platinum drug treatment via the cell cycle checkpoint response as opposed to the DNA repair processes; the increase in RAD51B protein foci (formed in response to DNA damage and thought to represent nuclear domains for HR repair) has been postulated to mediate cell cycle arrest in response to the platinum drugs, oxaliplatin and cisplatin. 39 …”
Section: Introductionmentioning
confidence: 99%