Enhanced adhesion/migration and induction of Pyk2 expression in K562 cells following imatinib exposure

Adelina Ovcharenko; Galit Granot; Oshrat Hershkovitz Rokah; Jennifer Park; Ofer Shpilberg; Pia Raanani

doi:10.1016/j.leukres.2013.10.005

Enhanced adhesion/migration and induction of Pyk2 expression in K562 cells following imatinib exposure

Adelina Ovcharenko, Galit Granot, Oshrat Hershkovitz Rokah, Jennifer Park, Ofer Shpilberg, Pia Raanani

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

6 Scopus citations

Abstract

Concern about extramedullary relapse (EMR) despite favorable response in the bone marrow has been raised with the use of imatinib for treatment of chronic myeloid leukemia (CML).In the present study we show an increase in adhesion, migration and invasion capabilities of the CML cell line K562 following imatinib administration. Imatinib induced upregulation of Pyk2 mRNA and protein levels. Pyk2 inhibition resulted in a reduction of K562 cells' adhesion and migration subsequent to imatinib treatment. This effect was similar to that shown by us previously with all trans retinoic acid (ATRA) in the acute promyelocytic leukemia (APL) cell line NB4.Our data pinpoint Pyk2 as a shared key mediator of targeted-therapy induced adhesion and migration and may implicate that targeting Pyk2 may serve as an effective therapeutic strategy to reduce EMR in APL and CML.

Original language	English
Pages (from-to)	1729-1736
Number of pages	8
Journal	Leukemia Research
Volume	37
Issue number	12
DOIs	https://doi.org/10.1016/j.leukres.2013.10.005
State	Published - Dec 2013
Externally published	Yes

Keywords

Adhesion
Chronic myeloid leukemia
Extramedullary disease
Imatinib
Migration
Pyk2

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10.1016/j.leukres.2013.10.005

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title = "Enhanced adhesion/migration and induction of Pyk2 expression in K562 cells following imatinib exposure",

abstract = "Concern about extramedullary relapse (EMR) despite favorable response in the bone marrow has been raised with the use of imatinib for treatment of chronic myeloid leukemia (CML).In the present study we show an increase in adhesion, migration and invasion capabilities of the CML cell line K562 following imatinib administration. Imatinib induced upregulation of Pyk2 mRNA and protein levels. Pyk2 inhibition resulted in a reduction of K562 cells' adhesion and migration subsequent to imatinib treatment. This effect was similar to that shown by us previously with all trans retinoic acid (ATRA) in the acute promyelocytic leukemia (APL) cell line NB4.Our data pinpoint Pyk2 as a shared key mediator of targeted-therapy induced adhesion and migration and may implicate that targeting Pyk2 may serve as an effective therapeutic strategy to reduce EMR in APL and CML.",

keywords = "Adhesion, Chronic myeloid leukemia, Extramedullary disease, Imatinib, Migration, Pyk2",

author = "Adelina Ovcharenko and Galit Granot and Rokah, {Oshrat Hershkovitz} and Jennifer Park and Ofer Shpilberg and Pia Raanani",

note = "Funding Information: The source of funding for this work was the Van Bits Scholarship donated by the Cancer Research Center, Tel-Aviv University , Israel and the Boaz Adar foundation from the Israel Cancer Association . ",

year = "2013",

month = dec,

doi = "10.1016/j.leukres.2013.10.005",

language = "אנגלית",

volume = "37",

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journal = "Leukemia Research",

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AU - Ovcharenko, Adelina

AU - Granot, Galit

AU - Rokah, Oshrat Hershkovitz

AU - Park, Jennifer

AU - Shpilberg, Ofer

AU - Raanani, Pia

N1 - Funding Information: The source of funding for this work was the Van Bits Scholarship donated by the Cancer Research Center, Tel-Aviv University , Israel and the Boaz Adar foundation from the Israel Cancer Association .

PY - 2013/12

Y1 - 2013/12

N2 - Concern about extramedullary relapse (EMR) despite favorable response in the bone marrow has been raised with the use of imatinib for treatment of chronic myeloid leukemia (CML).In the present study we show an increase in adhesion, migration and invasion capabilities of the CML cell line K562 following imatinib administration. Imatinib induced upregulation of Pyk2 mRNA and protein levels. Pyk2 inhibition resulted in a reduction of K562 cells' adhesion and migration subsequent to imatinib treatment. This effect was similar to that shown by us previously with all trans retinoic acid (ATRA) in the acute promyelocytic leukemia (APL) cell line NB4.Our data pinpoint Pyk2 as a shared key mediator of targeted-therapy induced adhesion and migration and may implicate that targeting Pyk2 may serve as an effective therapeutic strategy to reduce EMR in APL and CML.

AB - Concern about extramedullary relapse (EMR) despite favorable response in the bone marrow has been raised with the use of imatinib for treatment of chronic myeloid leukemia (CML).In the present study we show an increase in adhesion, migration and invasion capabilities of the CML cell line K562 following imatinib administration. Imatinib induced upregulation of Pyk2 mRNA and protein levels. Pyk2 inhibition resulted in a reduction of K562 cells' adhesion and migration subsequent to imatinib treatment. This effect was similar to that shown by us previously with all trans retinoic acid (ATRA) in the acute promyelocytic leukemia (APL) cell line NB4.Our data pinpoint Pyk2 as a shared key mediator of targeted-therapy induced adhesion and migration and may implicate that targeting Pyk2 may serve as an effective therapeutic strategy to reduce EMR in APL and CML.

KW - Adhesion

KW - Chronic myeloid leukemia

KW - Extramedullary disease

KW - Imatinib

KW - Migration

KW - Pyk2

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SN - 0145-2126

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EP - 1736

JO - Leukemia Research

JF - Leukemia Research

IS - 12

ER -

Enhanced adhesion/migration and induction of Pyk2 expression in K562 cells following imatinib exposure

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