Impact of intracellular chloride concentration on cisplatin accumulation in sensitive and resistant GLC4 cells

Salerno, Milena; Yahia, Dalila Ait; Dzamitika, Simplice; Vries, Elisabeth G.E. de; Pereira-Maia, Elene C.; Garnier‐Suillerot, Arlette

doi:10.1007/s00775-008-0430-3

Cited by 12 publications

(10 citation statements)

References 45 publications

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“…Cisplatin-resistant lung cancer cell lines with reduced platinum uptake have also been noted to have increased intracellular chloride96 or zinc content91, increased cell membrane rigidity97, increased sphingomyelin content97, and increased density of membrane lipid packing, with reduced long chain and unsaturated fatty acids98. These changes could potentially alter passive diffusion of cisplatin into cells or might reduce the activity of membrane transporters.…”

Section: 0 Drug Uptakementioning

confidence: 99%

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Stewart

2010

Critical Reviews in Oncology/Hematology

161

157

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While chemotherapy provides useful palliation, advanced lung cancer remains incurable since those tumors that are initially sensitive to therapy rapidly develop acquired resistance. Resistance may arise from impaired drug delivery, extracellular factors, decreased drug uptake into tumor cells, increased drug efflux, drug inactivation by detoxifying factors, decreased drug activation or binding to target, altered target, increased damage repair, tolerance of damage, decreased proapoptotic factors, increased antiapoptotic factors, or altered cell cycling or transcription factors. Factors for which there is now substantial clinical evidence of a link to small cell lung cancer (SCLC) resistance to chemotherapy include MRP (for platinum-based combination chemotherapy) and MDR1/P-gp (for non-platinum agents). SPECT MIBI and Tc-TF scanning appears to predict chemotherapy benefit in SCLC. In non-small cell lung cancer (NSCLC), the strongest clinical evidence is for taxane resistance with elevated expression or mutation of class III β-tubulin (and possibly α tubulin), platinum resistance and expression of ERCC1 or BCRP, gemcitabine resistance and RRM1 expression, and resistance to several agents and COX-2 expression (although COX-2 inhibitors have had minimal impact on drug efficacy clinically). Tumors expressing high BRCA1 may have increased resistance to platinums but increased sensitivity to taxanes. Limited early clinical data suggest that chemotherapy resistance in NSCLC may also be increased with decreased expression of cyclin B1 or of Eg5, or with increased expression of ICAM, matrilysin, osteopontin, DDH, survivin, PCDGF, caveolin-1, p21WAF1/CIP1, or 14-3-3sigma, and that IGF-1R inhibitors may increase efficacy of chemotherapy, particularly in squamous cell carcinomas. Equivocal data (with some positive studies but other negative studies) suggest that NSCLC tumors with some EGFR mutations may have increased sensitivity to chemotherapy, while K-ras mutations and expression of GST-pi, RB or p27kip1 may possibly confer resistance. While limited clinical data suggest that p53 mutations are associated with resistance to platinum-based therapies in NSCLC, data on p53 IHC positivity are equivocal. To date, resistance-modulating strategies have generally not proven clinically useful in lung cancer, although small randomized trials suggest a modest benefit of verapamil and related agents in NSCLC.

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Section: 0 Drug Uptakementioning

confidence: 99%

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Stewart

2010

Critical Reviews in Oncology/Hematology

161

157

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“…1 Recently, elevated intracellular chloride concentrations have been shown to be another possible mechanism of resistance. 4 The use of cisplatin is also limited because of its severe dose-limiting side effects that include nephrotoxicity, ototoxicity, and neurotoxicity. 1 In the past decade, only one new platinum drug, oxaliplatin, has been approved worldwide, and although it has shown potential for treating a range of cancers, it is only currently used for colorectal tumors.…”

Section: Introductionmentioning

confidence: 99%

Gold Nanoparticles for the Improved Anticancer Drug Delivery of the Active Component of Oxaliplatin

et al. 2010

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The platinum-based anticancer drugs cisplatin, carboplatin, and oxaliplatin are an important component of chemotherapy but are limited by severe dose-limiting side effects and the ability of tumors to develop resistance rapidly. These drugs can be improved through the use of drug-delivery vehicles that are able to target cancers passively or actively. In this study, we have tethered the active component of the anticancer drug oxaliplatin to a gold nanoparticle for improved drug delivery. Naked gold nanoparticles were functionalized with a thiolated poly(ethylene glycol) (PEG) monolayer capped with a carboxylate group. [Pt(1R,2R-diaminocyclohexane)(H2O)2]2NO3 was added to the PEG surface to yield a supramolecular complex with 280 (±20) drug molecules per nanoparticle. The platinum-tethered nanoparticles were examined for cytotoxicity, drug uptake, and localization in the A549 lung epithelial cancer cell line and the colon cancer cell lines HCT116, HCT15, HT29, and RKO. The platinum-tethered nanoparticles demonstrated as good as, or significantly better, cytotoxicity than oxaliplatin alone in all of the cell lines and an unusual ability to penetrate the nucleus in the lung cancer cells.

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“…According to the literature, treatment with cisplatin induces an increase of the intracellular Ca 2+ concentration [ 46 ], which is an important ion for the phospholipid membrane-binding activity of ANXA4. In contrast, cisplatin exposure also induces an elevation of the intracellular chloride concentration: [Cl − ] i [ 47 ]. Elevation of [Cl − ] i has been shown to prevent the aquation of 1 or 2 of the 2 chloride coordination sites in cisplatin, and only the aquated forms of cisplatin covalently bind to DNA.…”

Section: Resultsmentioning

confidence: 99%

Annexin A4 induces platinum resistance in a chloride-and calcium-dependent manner

et al. 2014

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Platinum resistance has long been a major issue in the treatment of various cancers. We previously reported that enhanced annexin A4 (ANXA4) expression, a Ca2+-regulated phospholipid-binding protein, induces chemoresistance to platinum-based drugs. In this study, we investigated the role of annexin repeats, a conserved structure of all the annexin family, responsible for platinum-resistance as well as the effect of knockdown of ANXA4. ANXA4 knockdown increased sensitivity to platinum-based drugs both in vitro and in vivo. To identify the domain responsible for chemoresistance, ANXA4 deletion mutants were constructed by deleting annexin repeats one by one from the C terminus. Platinum resistance was induced both in vitro and in vivo in cells expressing either full-length ANXA4 or the deletion mutants, containing at least one intact annexin repeat. However, cells expressing the mutant without any calcium-binding sites in the annexin repeated sequence, which is essential for ANXA4 translocation from the cytosol to plasma membrane, failed to acquire platinum resistance. After cisplatin treatment, the intracellular chloride ion concentration, whose channel is partly regulated by ANXA4, significantly increased in the platinum-resistant cells. These findings indicate that the calcium-binding site in the annexin repeat induces chemoresistance to the platinum-based drug by elevating the intracellular chloride concentration.

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Impact of intracellular chloride concentration on cisplatin accumulation in sensitive and resistant GLC4 cells

Cited by 12 publications

References 45 publications

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer

Gold Nanoparticles for the Improved Anticancer Drug Delivery of the Active Component of Oxaliplatin

Annexin A4 induces platinum resistance in a chloride-and calcium-dependent manner

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