Fludarabine Nucleoside Modulates Nuclear “Survival and Death” Proteins in Resistant Chronic Lymphocytic Leukemia Cells

Silke Henrich; Swetlana Mactier; Giles Best; Stephen P. Mulligan; Ben Crossett; Richard Ian Christopherson

doi:10.1080/15257770.2011.603716

Fludarabine Nucleoside Modulates Nuclear “Survival and Death” Proteins in Resistant Chronic Lymphocytic Leukemia Cells

Silke Henrich, Swetlana Mactier, Giles Best, Stephen P. Mulligan, Ben Crossett, Richard Ian Christopherson

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

The nuclear mechanisms by which fludarabine nucleoside (F-ara-A) induces apoptosis have been investigated in human MEC1 cells derived from B-cell chronic lymphocytic leukemia. Upon treatment of cells with F-ara-A (100 μM, 72 hours), 15 nuclear proteins changed in abundance by more than 2-fold. Nuclear proteins up-regulated included calmodulin (4.3-fold), prohibitin (3.9-fold), β-actin variant (3.7-fold), and structure-specific recognition protein 1 (3.7-fold); those downregulated included 60S ribosomal protein P2B (0.12-fold), fumarate hydratase (0.19-fold), splicing factor arginine/serine-rich 3 (0.35-fold), and replication protein A2 (0.42-fold). These changes in the levels of specific proteins promote survival or apoptosis; because the end result is apoptosis of MEC1 cells, apoptotic effects predominate.

Original language	English
Pages (from-to)	1181-1189
Number of pages	9
Journal	Nucleosides, Nucleotides and Nucleic Acids
Volume	30
Issue number	12
DOIs	https://doi.org/10.1080/15257770.2011.603716
Publication status	Published - Dec 2011
Externally published	Yes

Keywords

Apoptosis
Chronic lymphocytic leukemia
DIGE
Fludarabine
Nuclear proteome

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/15257770.2011.603716Licence: In Copyright

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title = "Fludarabine Nucleoside Modulates Nuclear “Survival and Death” Proteins in Resistant Chronic Lymphocytic Leukemia Cells",

abstract = "The nuclear mechanisms by which fludarabine nucleoside (F-ara-A) induces apoptosis have been investigated in human MEC1 cells derived from B-cell chronic lymphocytic leukemia. Upon treatment of cells with F-ara-A (100 μM, 72 hours), 15 nuclear proteins changed in abundance by more than 2-fold. Nuclear proteins up-regulated included calmodulin (4.3-fold), prohibitin (3.9-fold), β-actin variant (3.7-fold), and structure-specific recognition protein 1 (3.7-fold); those downregulated included 60S ribosomal protein P2B (0.12-fold), fumarate hydratase (0.19-fold), splicing factor arginine/serine-rich 3 (0.35-fold), and replication protein A2 (0.42-fold). These changes in the levels of specific proteins promote survival or apoptosis; because the end result is apoptosis of MEC1 cells, apoptotic effects predominate.",

keywords = "Apoptosis, Chronic lymphocytic leukemia, DIGE, Fludarabine, Nuclear proteome",

author = "Silke Henrich and Swetlana Mactier and Giles Best and Mulligan, {Stephen P.} and Ben Crossett and Christopherson, {Richard Ian}",

year = "2011",

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AU - Henrich, Silke

AU - Mactier, Swetlana

AU - Best, Giles

AU - Mulligan, Stephen P.

AU - Crossett, Ben

AU - Christopherson, Richard Ian

PY - 2011/12

Y1 - 2011/12

N2 - The nuclear mechanisms by which fludarabine nucleoside (F-ara-A) induces apoptosis have been investigated in human MEC1 cells derived from B-cell chronic lymphocytic leukemia. Upon treatment of cells with F-ara-A (100 μM, 72 hours), 15 nuclear proteins changed in abundance by more than 2-fold. Nuclear proteins up-regulated included calmodulin (4.3-fold), prohibitin (3.9-fold), β-actin variant (3.7-fold), and structure-specific recognition protein 1 (3.7-fold); those downregulated included 60S ribosomal protein P2B (0.12-fold), fumarate hydratase (0.19-fold), splicing factor arginine/serine-rich 3 (0.35-fold), and replication protein A2 (0.42-fold). These changes in the levels of specific proteins promote survival or apoptosis; because the end result is apoptosis of MEC1 cells, apoptotic effects predominate.

AB - The nuclear mechanisms by which fludarabine nucleoside (F-ara-A) induces apoptosis have been investigated in human MEC1 cells derived from B-cell chronic lymphocytic leukemia. Upon treatment of cells with F-ara-A (100 μM, 72 hours), 15 nuclear proteins changed in abundance by more than 2-fold. Nuclear proteins up-regulated included calmodulin (4.3-fold), prohibitin (3.9-fold), β-actin variant (3.7-fold), and structure-specific recognition protein 1 (3.7-fold); those downregulated included 60S ribosomal protein P2B (0.12-fold), fumarate hydratase (0.19-fold), splicing factor arginine/serine-rich 3 (0.35-fold), and replication protein A2 (0.42-fold). These changes in the levels of specific proteins promote survival or apoptosis; because the end result is apoptosis of MEC1 cells, apoptotic effects predominate.

KW - Apoptosis

KW - Chronic lymphocytic leukemia

KW - DIGE

KW - Fludarabine

KW - Nuclear proteome

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ER -

Fludarabine Nucleoside Modulates Nuclear “Survival and Death” Proteins in Resistant Chronic Lymphocytic Leukemia Cells

Abstract

Keywords

UN SDGs

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