Acquisition of Cisplatin-resistance in Malignant Mesothelioma Cells Abrogates Na&lt;sup&gt;&amp;plus;&lt;/sup&gt;,K&lt;sup&gt;&amp;plus;&lt;/sup&gt;,2Cl&lt;sup&gt;-;&lt;/sup&gt;-cotransport Activity and Cisplatin-induced Early Membrane Blebbing

Janson, Veronica; Andersson, Britta; Behnam‐Motlagh, Parviz; Engström, Karl Gunnar; Henriksson, Roger; Grankvist, Kjell

doi:10.1159/000149782

Cited by 14 publications

(27 citation statements)

References 38 publications

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“…Janson and coworkers have demonstrated that cisplatin resistance in malignant mesothelioma cells involves a marked reduction in the Na + ,K + ,2Cl -cotransport (NKCC1) activity [39]. However, the reduced NKCC1 activity was not important for the cisplatin resistance [39]. In agreement we find that NKCC activity counteracts ion and water loss during apoptosis [18].…”

Section: Cisplatin Resistance In Adherent Vs Non-adherent Cancer Cellssupporting

confidence: 86%

“…The reduced sensitivity to cisplatin in MDR EATC was correlated with a low activity of the volume-sensitive Cl -channel [18]. Janson and coworkers have demonstrated that cisplatin resistance in malignant mesothelioma cells involves a marked reduction in the Na + ,K + ,2Cl -cotransport (NKCC1) activity [39]. However, the reduced NKCC1 activity was not important for the cisplatin resistance [39].…”

Section: Cisplatin Resistance In Adherent Vs Non-adherent Cancer Cellsmentioning

confidence: 99%

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Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Tastesen

Holm

Møller³

et al. 2010

Cell Physiol Biochem

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Platinum compounds are used in the treatment of cancer. We demonstrate that cisplatin-induced (10 µM) apoptosis (caspase-3 activity) is pronounced within 18 hours in non-adherent Ehrlich ascites tumour cells (EATC), whereas there is no increase in caspase-3 activity in the adherent Ehrlich LettrÉ ascites tumour cells (ELA). Loss of KCl and cell shrinkage are hallmarks in apoptosis and has been shown in EATC. However, we find no reduction in cell volume and only a minor loss of K⁺ which is accompanied by net uptake of Na⁺ following 18 hours cisplatin exposure in ELA. Glutathione and taurine have previously been demonstrated to protect cells from apoptosis. We find, however, that increase or decrease in the cellular content of glutathione and taurine has no effect on cisplatin-induced cell death in EATC and ELA. Nevertheless, knock-down of the taurine transporter TauT leads to a significant increase in apoptosis in ELA following cisplatin exposure. We find that cytosolic accumulation of cisplatin is similar in EATC and ELA. However, the nuclear accumulation and DNA-binding of cisplatin is significant lower in ELA compared to EATC. We suggest three putative reasons for the observed cisplatin insensitivity in the adherent tumor cells (ELA) compared to the non-adherent tumor cells (EATC): less nuclear cisplatin accumulation, increased TauT activity, and decreased anion and water loss.

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Section: Cisplatin Resistance In Adherent Vs Non-adherent Cancer Cellssupporting

confidence: 86%

Section: Cisplatin Resistance In Adherent Vs Non-adherent Cancer Cellsmentioning

confidence: 99%

Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Tastesen

Holm

Møller³

et al. 2010

Cell Physiol Biochem

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“…The mesothelioma cell model P31 and its respective cisplatin-resistant subline P31/cis have been generously donated by K. Grankvist (Umeå University, Sweden). 48 The non-small-cell lung cancer cell model SW1573 with its MRP1-and LRP-overexpressing subline 2R120 and its P-gp-overexpressing subline 2R160 is from H. Broxterman (Department of Medical Oncology, Free University Hospital, Amsterdam, The Netherlands). 53 The ovarian carcinoma model A2780 with its cisplatin-selected subline A2780/cis was purchased from Sigma-Aldrich.…”

Section: Cell Lines and Culture Conditionsmentioning

confidence: 99%

Unsymmetric Mono- and Dinuclear Platinum(IV) Complexes Featuring an Ethylene Glycol Moiety: Synthesis, Characterization, and Biological Activity

et al. 2012

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Eight novel mononuclear and two dinuclear platinum(IV) complexes were synthesized and characterized by elemental analysis, one-and two-dimensional NMR spectroscopy, mass spectrometry, and reversed-phase HPLC (log k w ) and in one case by X-ray diffraction. Cytotoxicity of the compounds was studied in three human cancer cell lines (CH1, SW480, and A549) by means of the MTT assay, featuring IC 50 values to the low micromolar range. Furthermore a selected set of compounds was investigated in additional cancer cell lines (P31 and P31/cis, A2780 and A2780/cis, SW1573, 2R120, and 2R160) with regard to their resistance patterns, offering a distinctly different scheme compared to cisplatin. To gain further insights into the mode of action, drug uptake, DNA synthesis inhibition, cell cycle effects, and induction of apoptosis were determined for two characteristic substances.

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“…12 The fluorescein diacetate cytotoxicity test performed in parallel with the detection of oligonucleosomal DNA fragmentation using, for example, terminal deoxynucleotidyl transferase-mediated dUT nick-end labelling assay can be used as an end-point assay for cellular apoptosis. 13 …”

mentioning

confidence: 99%

“…However, in a cell model of acquired cisplatin resistance in malignant pleural mesothelioma cells we have previously shown that P31res1.2 cells have reduced NKCC1 activity and disrupted K + -regulation. 13 It cannot be excluded that these changes may affect caspase activity, as well as, for example, accumulation and intra-cellular trapping of cisplatin. Furthermore, both caspase-3 and caspase-7 can cleave DNA fragmentation factor 45/inhibitor of caspase-activated DNase (DFF45/ICAD) and release active DNA fragmentation factor 40/caspase-activated DNase nuclease (DFF40/CAD), which forms homo-oligomers and generates double-strand breaks in DNA.…”

mentioning

confidence: 99%

Resistance to caspase-8 and -9 fragments in a malignant pleural mesothelioma cell line with acquired cisplatin-resistance

2010

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Apoptotic cysteine–aspartate proteases (caspases) are essential for the progression and execution of apoptosis, and detection of caspase fragmentation or activity is often used as markers of apoptosis. Cisplatin (cis-diamminedichloroplatinum (II)) is a chemotherapeutic drug that is clinically used for the treatment of solid tumours. We compared a cisplatin-resistant pleural malignant mesothelioma cell line (P31res1.2) with its parental cell line (P31) regarding the consequences of in vitro acquired cisplatin-resistance on basal and cisplatin-induced (equitoxic and equiapoptotic cisplatin concentrations) caspase-3, -8 and -9 fragmentation and proteolytic activity. Acquisition of cisplatin-resistance resulted in basal fragmentation of caspase-8 and -9 without a concomitant increase in proteolytic activity, and there was an increased basal caspase-3/7 activity. Similarly, cisplatin-resistant non-small-cell lung cancer cells, H1299res, had increased caspase-3 and -9 content compared with the parental H1299 cells. In P31 cells, cisplatin exposure resulted in caspase-9-mediated caspase-3/7 activation, but in P31res1.2 cells the cisplatin-induced caspase-3/7 activation occurred before caspase-8 or -9 activation. We therefore concluded that in vitro acquisition of cisplatin-resistance rendered P31res1.2 cells resistant to caspase-8 and caspase-9 fragments and that cisplatin-induced, initiator-caspase independent caspase-3/7 activation was necessary to overcome this resistance. Finally, the results demonstrated that detection of cleaved caspase fragments alone might be insufficient as a marker of caspase activity and ensuing apoptosis induction.

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Acquisition of Cisplatin-resistance in Malignant Mesothelioma Cells Abrogates Na<sup>+</sup>,K<sup>+</sup>,2Cl<sup>-;</sup>-cotransport Activity and Cisplatin-induced Early Membrane Blebbing

Cited by 14 publications

References 38 publications

Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Pinpointing Differences in Cisplatin-induced Apoptosis in Adherent and Non-adherent Cancer Cells

Unsymmetric Mono- and Dinuclear Platinum(IV) Complexes Featuring an Ethylene Glycol Moiety: Synthesis, Characterization, and Biological Activity

Resistance to caspase-8 and -9 fragments in a malignant pleural mesothelioma cell line with acquired cisplatin-resistance

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