Human colon cancer cells surviving high doses of cisplatin or oxaliplatin in vitro are not defective in DNA mismatch repair proteins

Sergent, C; Franco, Noreli; Chapusot, Caroline; Lizard-Nacol, Sarab; Isambert, Nicolás; Correia, Maria; Chauffert, Bruno

doi:10.1007/s00280-002-0450-6

Cited by 43 publications

(27 citation statements)

References 19 publications

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“…Previously, we and others (reviewed in [31,32] have found I3C to be effective at inhibiting survival signalling in colorectal and other cell lines, but this is the first study to demonstrate increased efficacy when combined with platinum-based therapeutics. In agreement with the data presented in this study, oxaliplatin has previously been reported to induce apoptosis in SW480 [33] and G 2 -and S-phase arrest [34] in SW620 cell lines. We have also previously shown enhanced anti-proliferative effects of curcumin combined with oxaliplatin, to be associated with increased caspase 8 activity and altered expression of G 2 /M-and checkpoint-related cell cycle proteins, including p53, p21, survivin and cdc2 [35].…”

Section: Discussionsupporting

confidence: 82%

Indole-3-carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines

Howells

Neal²,

Brown³

et al. 2008

Biochemical Pharmacology

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Abstract.The primary aim of this study was to determine whether combination of the chemopreventive agent indole-3-carbinol with oxaliplatin would decrease proliferative index and invasive potential of human colorectal tumour cells.Combination of the agents resulted in a 170-fold decrease in proliferative capacity in SW480 and SW620 cell lines, which was approximately 6-fold greater than for oxaliplatin alone. Decreased proliferation was attributed to enhanced S-phase cell cycle arrest for SW480, and increased apoptosis for SW620 cells.The combined agents resulted in significantly increased E-cadherin levels in SW480 cells, and β-catenin levels in both cell lines (assessed by in-cell westerns). In SW480 cells confocal microscopy revealed an increase in membrane-associated β-catenin levels, with oxaliplatin treatments enhancing nuclear export and cytoplasmic localisation. In SW620 cells, all treatments increased membrane localisation of Ecadherin.Whilst both oxaliplatin and I3C decreased invasive capacity of SW480 cells, this was not further enhanced by the combined treatment.

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Section: Discussionsupporting

confidence: 82%

Indole-3-carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines

Howells

Neal²,

Brown³

et al. 2008

Biochemical Pharmacology

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“…When cisplatin-resistant clones were selected from a pure population of cisplatinsensitive, MMR-proficient A2780 cells, in all cases they had retained normal MMR repair capacity (Massey et al, 2003). Similarly, colon tumor cell lines selected for cisplatin resistance did not present with defects in DNA MMR proteins (Sergent et al, 2002). Finally, in Msh2-deficient murine intestinal enterocytes, only a slightly reduced apoptotic response to cisplatin could be observed that did not influence the overall survival of crypt cells (Sansom and Clarke, 2002), and indications for the involvement of the p73 pathway were not found.…”

Section: Discussionmentioning

confidence: 99%

Msh2 deficiency does not contribute to cisplatin resistance in mouse embryonic stem cells

Claij

Riele

2004

Oncogene

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Several reports have suggested that a defect in the DNA mismatch repair (MMR) system not only causes resistance to methylating agents but also confers low-level resistance to the chemotherapeutic drug cisplatin. Here we report that in a clonogenic assay, mouse embryonic stem (ES) cells deficient for the MMR protein MSH2 respond similarly as wild-type cells to cisplatin. Furthermore, restoring MSH2 expression in a cisplatin-resistant subclone selected from an Msh2 À/À cell population did not sensitize cells to cisplatin. To ascertain that our observations were not the result of a mutation in the Msh2 À/À cells that obscured the contribution of a defective MMR machinery to cisplatin resistance, we made use of the Cre-lox system to create a cell line in which the Msh2 gene can be conditionally inactivated. However, while de novo inactivation of Msh2 rendered cells tolerant to the methylating drug N-methyl-N 0 -nitro-N-nitrosoguanidine as expected, it did not alter the sensitivity to cisplatin. In addition, we were not able to derive cisplatin-resistant subclones from this freshly generated MMR-deficient cell line. Thus, in ES cells we did not find evidence for direct involvement of MMR deficiency in cisplatin resistance.

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“…The two cells lines not present significative differentiation at the level of DNA mismatch proteins as describes in [16,17]. Respect to oxidative damages both cellular lines present the similarity resistance to H 2 O 2 citotoxicity [17], and similar antioxidants enzyme activity like glutathione peroxidase [18].…”

Section: Cell Culturementioning

confidence: 99%

(2α,3β)‐2,3‐Dihydroxyolean‐12‐en‐28‐oic acid, a new natural triterpene from Olea europea, induces caspase dependent apoptosis selectively in colon adenocarcinoma cells

et al. 2006

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Triterpenoids are known to induce apoptosis and to be anti-tumoural. Maslinic acid, a pentacyclic triterpene, is present in high concentrations in olive pomace. This study examines the response of HT29 and Caco-2 colon-cancer cell lines to maslinicacid treatment. At concentrations inhibiting cell growth by 50-80% (IC50HT29 = 61 ± 1 lM, IC80HT29 = 76 ± 1 lM and IC50Caco-2 = 85 ± 5 lM, IC80Caco-2 = 116 ± 5 lM), maslinic acid induced strong G0/G1 cell-cycle arrest and DNA fragmentation, and increased caspase-3 activity. However, maslinic acid did not alter the cell cycle or induce apoptosis in the nontumoural intestine cell lines IEC-6 and IEC-18. Moreover, maslinic acid induced cell differentiation in colon adenocarcinoma cells. These findings support a role for maslinic acid as a tumour suppressant and as a possible new therapeutic tool for aberrant cell proliferation in the colon. In this report, we demonstrate for the first time that, in tumoural cancer cells, maslinic acid exerts a significant anti-proliferation effect by inducing an apoptotic process characterized by caspase-3 activation by a p53-independent mechanism, which occurs via mitochondrial disturbances and cytochrome c release.

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Human colon cancer cells surviving high doses of cisplatin or oxaliplatin in vitro are not defective in DNA mismatch repair proteins

Abstract: These results indicate that high-level resistance of human colon cancer cells to high doses of cisplatin and oxaliplatin does not seem to be related to acquired defects in the DNA MMR proteins.

Cited by 43 publications

References 19 publications

Indole-3-carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines

Indole-3-carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines

Msh2 deficiency does not contribute to cisplatin resistance in mouse embryonic stem cells

(2α,3β)‐2,3‐Dihydroxyolean‐12‐en‐28‐oic acid, a new natural triterpene from Olea europea, induces caspase dependent apoptosis selectively in colon adenocarcinoma cells

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