Cross-resistance between cisplatin, antimony potassium tartrate, and arsenite in human tumor cells.

Naredi, Peter; Heath, Dennis D.; Enns, Robert E.; Howell, Stephen B.

doi:10.1172/jci117768

Cited by 43 publications

(32 citation statements)

References 31 publications

(24 reference statements)

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“…Antisense clone as28 also grew slowly compared to wild-type 2008 while ASNA1 overexpressing clone s18 and the empty vector control displayed similar doubling times (Table I). wild-type and also resistant to antimonite and arsenite (4). To evaluate if ASNA1 is involved in RASP (Resistance to As, Sb and Pt), the ASNA1 expression in 2008/A was measured.…”

Section: Resultsmentioning

confidence: 99%

“…One important mechanism for resistance is reduction of intracellular platinum levels (3). Cisplatin resistant cells exhibit not only a low platinum content, but also a decreased accumulation of arsenite (4). These cells are cross resistant to arsenite, antimonite and cisplatin, termed the RASP-phenotype (Resistance to As, Sb and Pt) (4,5).…”

Section: Introductionmentioning

confidence: 99%

“…Cisplatin resistant cells exhibit not only a low platinum content, but also a decreased accumulation of arsenite (4). These cells are cross resistant to arsenite, antimonite and cisplatin, termed the RASP-phenotype (Resistance to As, Sb and Pt) (4,5). This suggests a common resistance mechanism that acts by either increased efflux or decreased influx of the drug.…”

Section: Introductionmentioning

confidence: 99%

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Increased sensitivity to platinating agents and arsenite in human ovarian cancer by downregulation of ASNA1

Hemmingsson

Nöjd²,

Kao³

et al. 2009

Oncol Rep

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Abstract. Platinating agents constitute the first line treatment for ovarian cancer but treatment failure is common because of intrinsic and acquired resistance. Cancer cells develop the RASP-phenotype (cross resistance against arsenite, antimonite and platinum) associated with decreased accumulation of cisplatin and arsenite. ASNA1 is a possible subunit of a transport system for cisplatin and arsenite due to homology to arsA, an ATPase in the E. coli ars-complex responsible for efflux of arsenite and antimonite. Eukaryotic ASNA1 is a targeting factor for membrane insertion of tail-anchored proteins involved in the secretory pathway and cellular stress responses. The purpose with this study was to evaluate if ASNA1 expression influenced cisplatin, carboplatin, oxaliplatin or arsenite sensitivity in ovarian cancer. Human ovarian cancer cell line 2008 was transfected with a sense or an antisense ASNA1 construct. ASNA1 downregulated and overexpressing clones were identified by Western blots. Cell growth and chemosensitivity was determined by the MTT assay. Downregulated ASNA1 expression was associated with retarded growth and increased sensitivity to cisplatin, carboplatin, oxaliplatin and arsenite whereas the cisplatin resistant 2008/ A overexpresses ASNA1. These observations support the hypothesis that ASNA1 is a target to overcome platinum resistance in ovarian cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increased sensitivity to platinating agents and arsenite in human ovarian cancer by downregulation of ASNA1

Hemmingsson

Nöjd²,

Kao³

et al. 2009

Oncol Rep

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“…Emerging evidence has shown that mechanisms involved in copper homeostasis play important roles in platinum transportation through cells (Komatsu et al, 2000;Ishida et al, 2002;Samimi et al, 2003). One of the earliest hints that copper homeostasis mechanisms might be involved in resistance to the platinum drugs was the observation that cells resistant to platinum drugs are cross-resistant with other metal or metalloid-containing agents (Naredi et al, 1995;Shen et al, 1998). In our oxaliplatin model, we found that S3 cells were cross-resistant to copper sulphate and arsenic trioxide (resistance index, 2 and 4.7, respectively) ( Table 1).…”

Section: Discussionmentioning

confidence: 99%

Combined modalities of resistance in an oxaliplatin-resistant human gastric cancer cell line with enhanced sensitivity to 5-fluorouracil

Chen

Tsou

et al. 2007

Br J Cancer

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To identify mechanisms underlying oxaliplatin resistance, a subline of the human gastric adenocarcinoma TSGH cell line, S3, was made resistant to oxaliplatin by continuous selection against increasing drug concentrations. Compared with the parental TSGH cells, the S3 subline showed 58-fold resistance to oxaliplatin; it also displayed 11-, 2-, and 4.7-fold resistance to cis-diammine-dichloroplatinum (II) (CDDP), copper sulphate, and arsenic trioxide, respectively. Interestingly, S3 cells were fourfold more susceptible to 5-fluorouracilinduced cytotoxicity due to downregulation of thymidylate synthase. Despite elevated glutathione levels in S3 cells, there was no alteration of resistant phenotype to oxaliplatin or CDDP when cells were co-treated with glutathione-depleting agent, l-buthionine-(S,R)-sulphoximine. Cellular CDDP and oxaliplatin accumulation was decreased in S3 cells. In addition, amounts of oxaliplatin-and CDDP -DNA adducts in S3 cells were about 15 and 40% of those seen with TSGH cells, respectively. Western blot analysis showed increased the expression level of copper transporter ATP7A in S3 cells compared with TSGH cells. Partial reversal of the resistance of S3 cells to oxaliplatin and CDDP was observed by treating cell with ATP7A-targeted siRNA oligonucleotides or P-type ATPaseinhibitor sodium orthovanadate. Besides, host reactivation assay revealed enhanced repair of oxaliplatin-or CDDP-damaged DNA in S3 cells compared with TSGH cells. Together, our results show that the mechanism responsible for oxaliplatin and CDDP resistance in S3 cells is the combination of increased DNA repair and overexpression of ATP7A. Downregulation of thymidylate synthase in S3 cells renders them more susceptible to 5-fluorouracil-induced cytotoxicity. These findings could pave ways for future efforts to overcome oxaliplatin resistance.

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“…Certain cisplatin-resistant cell lines demonstrate cross-resistance to metals that include cadmium, antimony and arsenite (19). The identification of cross-resistant metals aids the evaluation of the mechanism underlying cisplatin resistance and metal transport systems.…”

Section: Discussionmentioning

confidence: 99%

Utilization of arsenic trioxide as a treatment of cisplatin-resistant non-small cell lung cancer PC-9/CDDP and PC-14/CDDP cells

et al. 2015

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Abstract. Cisplatin is a commonly used drug in combination chemotherapy. However, various malignant tumors frequently acquire resistance to cisplatin. Arsenic trioxide (ATO) has been approved as a chemotherapeutic drug for the treatment of acute promyelocytic leukemia, and the combination of ATO and cisplatin has been revealed to demonstrate synergistic effects in ovarian and small cell lung cancer cells. Thus, it was hypothesized that ATO may also be active against cisplatin-resistant non-small cell lung cancer (NSCLC) PC-9/CDDP and PC-14/CDDP cells. The present study also evaluated the effects of ATO on the cisplatin-sensitive NSCLC PC-9 and PC-14 cell lines. Notably, ATO demonstrated a markedly decreased IC 50 in the cisplatin-resistant PC-9/CDDP and PC-14/CDDP cells compared with the IC 50 in the cisplatin-sensitive parental PC-9 and PC-14 cells.

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Cross-resistance between cisplatin, antimony potassium tartrate, and arsenite in human tumor cells.

Cited by 43 publications

References 31 publications

Increased sensitivity to platinating agents and arsenite in human ovarian cancer by downregulation of ASNA1

Increased sensitivity to platinating agents and arsenite in human ovarian cancer by downregulation of ASNA1

Combined modalities of resistance in an oxaliplatin-resistant human gastric cancer cell line with enhanced sensitivity to 5-fluorouracil

Utilization of arsenic trioxide as a treatment of cisplatin-resistant non-small cell lung cancer PC-9/CDDP and PC-14/CDDP cells

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