Cisplatin resistance: Preclinical findings and clinical implications

Köberle, Beate; Tomičić, Maja; Usanova, Svetlana; Kaina, Bernd

doi:10.1016/j.bbcan.2010.07.004

Cited by 246 publications

(263 citation statements)

References 150 publications

Supporting

Mentioning

244

Contrasting

Unclassified

Order By: Relevance

“…5,16,22,35 Here, we found that this resistance phenotype correlate with gene expression regulation of several Figure 6 Caspase role in cell death elicited by PDIA4 and PDIA6 knockdown and CDDP. R1, R2 and R3 cells were treated only with siRNA PDIA6 for 48 h followed by 2 h of 50 mM caspase inhibitor Z-VAD or Z-LEVD and/or 48 h of 25 mM CDDP treatment.…”

Section: Discussionmentioning

confidence: 85%

The protein disulfide isomerases PDIA4 and PDIA6 mediate resistance to cisplatin-induced cell death in lung adenocarcinoma

et al. 2014

View full text Add to dashboard Cite

Intrinsic and acquired chemoresistance are frequent causes of cancer eradication failure. Thus, long-term cis-diaminedichloroplatine(II) (CDDP) or cisplatin treatment is known to promote tumor cell resistance to apoptosis induction via multiple mechanisms involving gene expression modulation of oncogenes, tumor suppressors and blockade of pro-apoptotic mitochondrial membrane permeabilization. Here, we demonstrate that CDDP-resistant non-small lung cancer cells undergo profound remodeling of their endoplasmic reticulum (ER) proteome (480 proteins identified by proteomics) and exhibit a dramatic overexpression of two protein disulfide isomerases, PDIA4 and PDIA6, without any alteration in ER-cytosol Ca 2 þ fluxes. Using pharmacological and genetic inhibition, we show that inactivation of both proteins directly stimulates CDDP-induced cell death by different cellular signaling pathways. PDIA4 inactivation restores a classical mitochondrial apoptosis pathway, while knockdown of PDIA6 favors a non-canonical cell death pathway sharing some necroptosis features. Overexpression of both proteins has also been found in lung adenocarcinoma patients, suggesting a clinical importance of these proteins in chemoresistance.

show abstract

Section: Discussionmentioning

confidence: 85%

The protein disulfide isomerases PDIA4 and PDIA6 mediate resistance to cisplatin-induced cell death in lung adenocarcinoma

et al. 2014

View full text Add to dashboard Cite

show abstract

“…S1P acts as second messenger intracellularly as well as a ligand for membrane-bound G-proteincoupled receptors, and it plays an important role in regulating central cellular processes, such as cell growth, cell apoptosiss, differentiation and motility (Köberle et al, 2010;Modra., 2006;Bieberich E, 2008;Reynolds CP., 2004) by up-regulating several antiapoptotic pathways including phosphatidy-linositol-kinase or NF-κB.…”

Section: Discussionmentioning

confidence: 99%

“…However, the efficacy of cisplatin is often limited because some tumors are intrinsically resistant to anti-tumor drugs, while in others resistance is selected for during the course of therapy (Köberle et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Reversion of Multidrug Resistance by SKI-II in SGC7901/DDP Cells and Exploration of Underlying Mechanisms

Zhu¹,

Zhu²,

Cai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

In order to investigate whether SKI-II could reverse drug resistance and its possible mechanisms, we treated SGC7901/DDP cells with SKI-II or SKI-II in combination with DDP. Then cell growth, apoptosis, micromorphological changes, and expression of SphK1, P-gp, NF-κB, Bcl-2 and Bax were assessed by MTT assay, flow cytometry, electron microscopy, immunocytochemistry and Western blot assay respectively. SGC7901/DDP cells were insensitive to cisplatin 2.5mg/L, but when pretreated with SKI-II, their proliferation was inhibited by cisplatin 2.5mg/L significantly, the inhibition rate increasing with time and dose. The apoptosis rate was also significantly elevated. Expression of SphK1 and P-gp was decreased significantly, Pearson correlation analysis showing significant correlation between the two (r=0.595, P<0.01). Expression of NF-κB and Bcl-2 was decreased significantly,while that of Bax was increased, compared to the control group. There were significant correlations between SphK1 and NF-κB(r=0.723, P<0.01), NF-κB and Bcl-2(r=0.768, P<0.01). All these data indicated that SKI-II could reverse drug resistance of SGC7901/DDP to cisplatin by down-regulating expression of P-gp and up-regulating apoptosis through down-regulation of SphK1. The increased apoptotic sensitivity of SGC7901/ DDP to cisplatin was due to the decreasing proportion of Bcl-2/Bax via down-regulating NF-κB.

show abstract

“…The two major problems associated with the use of cisplatin derivatives are the severe toxic side effects (11)(12)(13)(14)(15) and the intrinsic or acquired resistance manifested in various types of cancers (16). Therefore, in recent decades, a large number of new metal-based complexes have been developed and tested (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Antiproliferative Activity of Gold(III) Complexes with Esters of Cyclohexyl-Functionalized Ethylenediamine-N,N’-Diacetate

Pantelić

Stanojković

Zmejkovski

et al. 2017

Serbian Journal of Experimental and Clinical Research

View full text Add to dashboard Cite

Six gold(III) complexes with esters of cyclohexyl-functionalized ethylenediamine-N,N'-diacetate, general formula [AuCl 2 {(S,S)-R 2 eddch}]PF 6 , [(S,S)-eddch = (S,S)-ethylenediamine-N,N'-di-2-(3-cyclohexyl)propanoate, R = Me, Et,[1][2][3][4][5][6], respectively], were tested against cancer cell lines such as human melanoma Fem-x, human colon carcinoma LS174T and non-small cell lung carcinoma A549 as well as a non-cancerous human embryonic lung fi broblasts [3][4] SAŽETAK Šest kompleksa zlata(III) sa cikloheksil-funkcionalizovanim estrima etilendiamin-N,N'-diacetata, opšte formule [AuCl 2 {(S,S)-R 2 eddch}]PF 6 , ((S,S)-eddch = (S,S)-etilendiamin-N,N'-di-2-(3-cicloheksil)propanoat, R = Me, Et, n-Pr, n-Bu, i-Bu, i-Am, 1-6), ispitivano je na humanim ćelijskim linijama malignog melanoma Fem-x, karcinoma debelog creva LS174T, karcinoma pluća A549 kao i normalnim ćeli-jama MRC-5 (fetalni plućni fi broblast) korišćenjem

show abstract

Cisplatin resistance: Preclinical findings and clinical implications

Cited by 246 publications

References 150 publications

The protein disulfide isomerases PDIA4 and PDIA6 mediate resistance to cisplatin-induced cell death in lung adenocarcinoma

The protein disulfide isomerases PDIA4 and PDIA6 mediate resistance to cisplatin-induced cell death in lung adenocarcinoma

Reversion of Multidrug Resistance by SKI-II in SGC7901/DDP Cells and Exploration of Underlying Mechanisms

Antiproliferative Activity of Gold(III) Complexes with Esters of Cyclohexyl-Functionalized Ethylenediamine-N,N’-Diacetate

Contact Info

Product

Resources

About