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Activity of Bortezomib in Glioblastoma

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Activity of Bortezomib in Glioblastoma ANTICANCER RESEARCH 26: 4499-4504 (2006) Activity of Bortezomib in Glioblastoma JAN STYCZYNSKI1*, DOROTA OLSZEWSKA-SLONINA2*, BEATA KOLODZIEJ1, MALGORZATA NAPIERAJ1 and MARIUSZ WYSOCKI1 1Department of Pediatric Hematology and Oncology, Laboratory of Clinical and Experimental Oncology, 2Department of Medical Biology, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland Abstract. Background: Chemotherapy is the commonly accepted of substrate polyubiquinated proteins, while normal activity standard therapy for most types of brain tumor, especially in rapidly clears them from the cell. Alteration of the levels of medulloblastoma, primitive neuroectodermal tumor and these cellular proteins leads to inhibition of proliferation, astrocytoma. However, no efficient therapy has been established migration and angiogenesis and to the promotion of to date for glioblastoma multiforme. The aim of the present study apoptosis of cancer cells. was to analyze the activity of bortezomib in glioblastoma cell lines Bortezomib (formerly PS-341, Figure 1) is an extremely in comparison with that in a pediatric acute lymphoblastic potent and selective proteasome inhibitor that showed leukemia cell line. Materials and Methods: Glioblastoma strong activity in in vitro and in vivo laboratory studies multiforme T98G, glioblastoma-astrocytoma U373M and T- against many solid and hematologic tumor types. Moreover, lineage acute lymphoblastic leukemia CCRF-CEM cell lines were bortezomib, mainly by inhibition of the NF-kappaB used. Proteasome inhibitor, bortezomib and 14 other anticancer pathway, had a chemosensitizing effect when administered drugs were tested using the MTT assay. Results: Compared to the together with other antitumoral drugs (2). Bortezomib is a acute lymphoblastic cell line, both glioblastoma cell lines showed biologically active agent, producing predictable, dose- relatively good sensitivity to bortezomib, as well as to cisplatin, related and reversible proteasome inhibition; it has shown carboplatin, etoposide and actinomycin-D. The lines showed antitumor activity in various malignancies and was the first intermediate sensitivity to thiotepa and daunorubicin, but were proteasome inhibitor to be used in clinical practice. Several highly resistant to first-line drugs used in the therapy of acute trials demonstrated that bortezomib is relatively well- lymphoblastic leukemia, such as prednisolone, L-asparaginase, tolerated, causing manageable non-hematological and vincristine, doxorubicin and cytarabine. Bortezomib, which is not hematological toxicity. Clinical phase I, II and III studies, a substrate for PGP and MRP1, did not show cross resistance to showed good tolerance of bortezomib and high response drugs transported by these proteins. Conclusion: Our results rates in refractory multiple myeloma patients (3, 4). It was support the necessity for further research on the role of bortezomib used as a single agent and in combination with in the therapy of glioblastoma. chemotherapeutic drugs, showing potentiation of the effect. In variety of other hematological malignancies and solid The proteasome is an ubiquituous enzyme complex that tumors, phase I and II studies with bortezomib alone or in plays a critical role in the degradation of many proteins combination with other drugs have produced encouraging involved in cell cycle regulation, apoptosis and angiogenesis results, both in children and adults (5-8), for carcinomas of (1). Inhibition of the 26S proteasome permits accumulation the breast, lung (9, 10), colon (11), bladder (3), ovary (12), pancreas (13) and prostate (12), melanoma (14), thyroid carcinoma (15) and metastatic neuroendocrine tumors (16). The objective of this study was the evaluation of the *Both authors contributed equally to the study. activity of bortezomib and 14 other anticancer drugs in glioblastoma cell lines, in comparison with that of childhood Correspondence to: Jan Styczynski, MD, Ph.D., Department of acute lymphoblastic leukemia CCRF-CEM cell line. Pediatric Hematology and Oncology, Collegium Medicum, Nicolaus Copernicus University, ul. Curie-Sklodowskiej 9, 85-094 Bydgoszcz, Poland. Tel: +48 52 585 4860, Fax: +48 52 585 4867, e- Materials and Methods mail: [email protected] Cell lines. Glioblastoma (T98G, U373MG) and T-lineage acute Key Words: Brain tumor, drug resistance, drug sensitivity, MTT lymphoblastic leukemia (CCRF-CEM) cell lines were analyzed. assay. Both brain tumor cell lines were maintained in EMEM (EBSS, 0250-7005/2006 $2.00+.40 4499 ANTICANCER RESEARCH 26: 4499-4504 (2006) Table I. Drug sensitivity and resistance of cell lines. Drug IC50 (mean±SD) CCRF-CEM T98G U373MG Bortezomib 18.5±4.3 28.9±4.5 48.2±12.3 RR=1.56 RR=2.6 (p<0.01) (p<0.01) Cisplatin 6.8±1.4 6.7±4.5 19.9±9.7 RR=0.99 (ns) RR=2.9 (p<0.01) Carboplatin 33.6±33.7 54.4±38.4 29.1±13.6 RR=1.6 (ns) RR=0.8 (ns) Etoposide 0.38±0.11 0.45±0.44 0.49±0.22 RR=1.2 (ns) RR=1.3 (ns) Figure 1. Chemical structure of bortezomib. Actinomycin-D 0.04±0.03 0.1±0.12 0.07±0.07 RR=2.5 (ns) RR=1.7 (ns) Thiotepa 1.01±0.17 9.74±4.96 8.59±6.78 RR=9.5 RR=8.4 (p<0.001) (p<0.05) Sigma, Munich, Germany) medium supplemented with 2 mM Daunorubicin 0.1±0.1 0.69±0.25 0.39±0.09 glutamine (Sigma), 1 mM non-essential amino acids (NEAA, RR=6.9 RR=3.9 Sigma), 1% sodium pyruvate (NaP, Sigma) and 10% fetal bovine (p<0.001) (p<0.001) serum (FBS, Gibco BRL, Paisley, UK). For seeding, 0.25% Cladribine 0.02±0.01 >40 0.9±0.22 trypsin/EDTA was used. The culture was carried out under RR>2000 RR=45 (p<0.001) (p<0.001) conditions of 5% CO2, 37ÆC and 95% humidity. The culture medium for CCRF-CEM cell line contained RPMI 1640 medium Arsenic trioxide 6.8±3.2 >20 >20 (Sigma), supplemented with 2 mM glutamine and 20% FBS. Both RR>2.9 RR>2.9 (p<0.001) (p<0.001) culture media were supplemented with 100 U/ml penicilin (Polfa Topotecan <0.097 0.2±0.01 21.36±18.93 Tarchomin, Poland), 100 Ìg/ml streptomycin (Polfa Tarchomin), RR>2 RR>220 200 Ìg/ml gentamycin (Krka, Nove mesto, Slovenia) and 0.125 (p<0.001) (p<0.001) Ìg/ml amphotericine B (Fungizone, Brisol-Myers Squibb, Ruel- Prednisolone 1.01±0.98 >250 >250 Malmaison, France). RR>247.5 RR>247.5 (p<0.001) (p<0.001) Drugs. The following 15 drugs were used: bortezomib (Velcade, Vincristine 0.09±0.03 7.19±2.36 8.23±2.28 Janssen Pharmaceutica N.V., Beerse, Belgium, concentrations RR=79.8 RR=91.4 tested: 0.19-200 nM), prednisolone (Jelfa, Jelenia Gora, Poland, (p<0.001) (p<0.001) 0.0076-250 Ìg/ml), vincristine (Gedeon Richter, Budapest, Hungary, L-asparaginase 0.1±0.08 0.97±0.71 2.67±2.12 0.019-20 Ìg/ml), L-asparaginase (Medac, Hamburg, Germany, RR=9.7 RR=26.7 0.0032-10 IU/ml), daunorubicin (Rhone-Poulenc Rorer, Montrouge, (p<0.001) (p<0.001) France, 0.0019-2 Ìg/ml), doxorubicin (Pharmacia Italia S.p.A., Doxorubicin 0.08±0.02 5.2±1.2 6.9±1.6 Milan, Italy, 0.031-40 Ìg/ml), actinomycin-D (Lyovac, MSD, Viena, RR=65 RR=86 (p<0.001) (p<0.001) Austria, 0.0048-5 Ìg/ml), cytarabine (Upjohn, Puurs, Belgium, 0.24- Cytarabine <0.24 67.8±46.7 >250 250 Ìg/ml), cladribine (Bioton, Warsaw, Poland, 0.0004-40 Ìg/ml), RR>282 RR>1041 cisplatin (Pliva-Lachema, Brno, Czech Republic, 0.97-100 Ìg/ml), (p<0.01) (p<0.001) carboplatin (Pliva-Lachema, 0.48-500 Ìg/ml), etoposide (Bristol- Myers Squibb, Sermoneta, Italy, 0.048-50 Ìg/ml), thiotepa (Lederle, RR (relative resistance)-ratio of mean values of IC50 of brain tumor Wolfratshausen, Germany, 0.032-100 Ìg/ml), arsenic trioxide cell line and leukemic CCRF-CEM cell line. P-value was calculated (Sigma, 0.019-20 ÌM), topotecan (Glaxo Smith Kline, Brentford, using the Student’s t-test. Concentration is given in nM for bortezomib, UK, 0.097-100 Ìg/ml). Before the assay was performed, most drug ÌM for arsenic trioxide, IU/ml for L-asparaginase and in Ìg/ml for the stock solutions were stored frozen in small aliquots at –20ÆC, except rest of the drugs. cladribine, cisplatin and carboplatin, which were stored at +4ÆC. Stock solutions were prepared in water for injection; further dilution was made in respective media. The MTT assay. Cellular drug resistance was tested by means of the resistance (RR) between cell lines for each drug was calculated as a MTT assay. The procedure of the assay was described previously ratio of mean value of IC50 for this drug in tested cell lines. (17). The drug concentration that was inhibitory to 50% of the cells (IC50) was calculated from the dose-response curve and was used as Statistical analysis. The t-test for independent samples was used to a measure for in vitro drug resistance in each sample. Results were compare differences in drug resistance between groups. The compared between respective cell lines. At least four independent correlation between cytotoxicity of drugs was determined by experiments were performed for each cell line. The relative Spearman’s rho coefficient. 4500 Styczynski et al: Activity of Bortezomib in Glioblastoma Results Bortezomib was only 1.56-2.6-fold less active in the glioblastoma cell lines when compared to the CCRF-CEM cell line. The leukemic cell line was the most drug-sensitive cell line for all tested drugs, with possible exception to cisplatin and carboplatin (Table I). These two drugs showed good activity against both brain tumor cell lines. Actinomycin-D and etoposide also showed good activity and were only 1.2- to 2.5-fold less cytotoxic against malignant brain tumor cells, in comparison with the leukemic cell line.
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