Imatinib increases apoptosis index through modulation of survivin subcellular localization in the blast phase of CML cells

Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the hi...

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Published inLeukemia research Vol. 36; no. 12; pp. 1510 - 1516
Main Authors Bernardo, Paula Sabbo, Reis, Flaviana Ruade de Souza, Maia, Raquel Ciuvalschi
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.12.2012
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ISSN0145-2126
1873-5835
1873-5835
DOI10.1016/j.leukres.2012.08.014

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Abstract Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the high apoptosis index induced by imatinib was associated with the survivin predominantly in the nucleus. In the Lucena cell line, the low apoptosis index induced by imatinib was associated with a cytoplasmatic survivin localization. Pgp and survivin might be subject to the same molecular regulation, and therefore represent a therapeutic target in the blast phase of CML.
AbstractList Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the high apoptosis index induced by imatinib was associated with the survivin predominantly in the nucleus. In the Lucena cell line, the low apoptosis index induced by imatinib was associated with a cytoplasmatic survivin localization. Pgp and survivin might be subject to the same molecular regulation, and therefore represent a therapeutic target in the blast phase of CML.
Abstract Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the high apoptosis index induced by imatinib was associated with the survivin predominantly in the nucleus. In the Lucena cell line, the low apoptosis index induced by imatinib was associated with a cytoplasmatic survivin localization. Pgp and survivin might be subject to the same molecular regulation, and therefore represent a therapeutic target in the blast phase of CML.
Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the high apoptosis index induced by imatinib was associated with the survivin predominantly in the nucleus. In the Lucena cell line, the low apoptosis index induced by imatinib was associated with a cytoplasmatic survivin localization. Pgp and survivin might be subject to the same molecular regulation, and therefore represent a therapeutic target in the blast phase of CML.Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two blast phase of chronic myeloid leukemia (CML) cell lines: K562 P-glycoprotein (Pgp)-negative, and Lucena, Pgp-positive. In K562 cell line, the high apoptosis index induced by imatinib was associated with the survivin predominantly in the nucleus. In the Lucena cell line, the low apoptosis index induced by imatinib was associated with a cytoplasmatic survivin localization. Pgp and survivin might be subject to the same molecular regulation, and therefore represent a therapeutic target in the blast phase of CML.
Author Bernardo, Paula Sabbo
Maia, Raquel Ciuvalschi
Reis, Flaviana Ruade de Souza
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Issue 12
Keywords P-glycoprotein
Imatinib
Chronic myeloid leukemia
Survivin
Subcellular localization
Language English
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Snippet Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in two...
Abstract Using MTT, Annexin V/flow cytometry, immunocytochemistry, subcellular fractionation, and Western blotting assays we analyzed the effect of imatinib in...
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StartPage 1510
SubjectTerms Annexin A5 - metabolism
Annexin V
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Apoptosis - genetics
ATP-Binding Cassette, Sub-Family B, Member 1 - genetics
ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism
Benzamides
Blast
Blast Crisis - drug therapy
Blast Crisis - genetics
Blast Crisis - pathology
Blotting, Western
Cell Nucleus - metabolism
Cell Nucleus - pathology
Cell Survival - drug effects
Chronic myeloid leukemia
Cytoplasm - metabolism
Cytoplasm - pathology
Flow Cytometry
Gene Expression Regulation, Neoplastic
Hematology, Oncology and Palliative Medicine
Humans
Imatinib
Imatinib Mesylate
Immunocytochemistry
Immunohistochemistry
Inhibitor of Apoptosis Proteins - genetics
Inhibitor of Apoptosis Proteins - metabolism
K562 Cells
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology
Nuclei
P-Glycoprotein
Piperazines - pharmacology
Pyrimidines - pharmacology
Subcellular localization
Survivin
Tumor cell lines
Western blotting
Title Imatinib increases apoptosis index through modulation of survivin subcellular localization in the blast phase of CML cells
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https://dx.doi.org/10.1016/j.leukres.2012.08.014
https://www.ncbi.nlm.nih.gov/pubmed/22975581
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https://www.proquest.com/docview/1257740292
Volume 36
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