Korean J Hematol 2012; 47(3):
Published online September 25, 2012
https://doi.org/10.5045/kjh.2012.47.3.219
© The Korean Society of Hematology
1Department of Laboratory Medicine, Konkuk University School of Medicine, Seoul, Korea.
2Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
3Department of Laboratory Medicine, Seoul National University College of Medicine, Seoul, Korea.
4Korean Cell Line Bank, Laboratory of Cell Biology, Cancer Research Center and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Correspondence to : Correspondence to Dong Soon Lee, M.D., Ph.D. Department of Laboratory Medicine, Seoul National University College of Medicine, 101, Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Tel: +82-2-2072-3986, Fax: +82-2-747-0359, soonlee@plaza.snu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Granulocyte-colony stimulating factor (G-CSF) is extensively used to improve neutrophil count during anti-cancer chemotherapy. We investigated the effects of G-CSF on several leukemic cell lines and screened for the expression of the G-CSF receptor (G-CSFR) in various malignant cells.
We examined the effects of the most commonly used commercial forms of G-CSF (glycosylated lenograstim and nonglycosylated filgrastim) on various leukemic cell lines by flow cytometry. Moreover, we screened for the expression of G-CSFR mRNA in 38 solid tumor cell lines by using real-time PCR.
G-CSF stimulated proliferation (40-80% increase in proliferation in treated cells as compared to that in control cells) in 3 leukemic cell lines and induced differentiation of
The results of the present study show that therapeutic G-CSF might stimulate the proliferation and differentiation of malignant cells with G-CSFR expression, suggesting that prescreening for G-CSFR expression in primary tumor cells may be necessary before using G-CSF for treatment.
Keywords G-CSF, Differentiation, Proliferation, Solid tumor, AML
Korean J Hematol 2012; 47(3): 219-224
Published online September 25, 2012 https://doi.org/10.5045/kjh.2012.47.3.219
Copyright © The Korean Society of Hematology.
Hee Won Moon1,#, Tae Young Kim2,#, Bo Ra Oh2, Sang Mee Hwang3, Jiseok Kwon2, Ja-Lok Ku4, and Dong Soon Lee2,3*
1Department of Laboratory Medicine, Konkuk University School of Medicine, Seoul, Korea.
2Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
3Department of Laboratory Medicine, Seoul National University College of Medicine, Seoul, Korea.
4Korean Cell Line Bank, Laboratory of Cell Biology, Cancer Research Center and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Correspondence to: Correspondence to Dong Soon Lee, M.D., Ph.D. Department of Laboratory Medicine, Seoul National University College of Medicine, 101, Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Tel: +82-2-2072-3986, Fax: +82-2-747-0359, soonlee@plaza.snu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Granulocyte-colony stimulating factor (G-CSF) is extensively used to improve neutrophil count during anti-cancer chemotherapy. We investigated the effects of G-CSF on several leukemic cell lines and screened for the expression of the G-CSF receptor (G-CSFR) in various malignant cells.
We examined the effects of the most commonly used commercial forms of G-CSF (glycosylated lenograstim and nonglycosylated filgrastim) on various leukemic cell lines by flow cytometry. Moreover, we screened for the expression of G-CSFR mRNA in 38 solid tumor cell lines by using real-time PCR.
G-CSF stimulated proliferation (40-80% increase in proliferation in treated cells as compared to that in control cells) in 3 leukemic cell lines and induced differentiation of
The results of the present study show that therapeutic G-CSF might stimulate the proliferation and differentiation of malignant cells with G-CSFR expression, suggesting that prescreening for G-CSFR expression in primary tumor cells may be necessary before using G-CSF for treatment.
Keywords: G-CSF, Differentiation, Proliferation, Solid tumor, AML
Expression of G-CSFR in hematologic malignancies and solid tumors using real-time PCR. Among hematologic malignancies, Kasumi-1 and K562 expressed G-CSFR mRNA whereas CTV-1 and U266 did not. Among 38 solid tumor cell lines, 5 cell lines (13.1%) expressed G-CSFR mRNA. The G-CSFR expression of each cell type was normalized to GAPDH expression. The relative expressions were presented as relative ratios compared to gene expression in Kasumi-1 cells (set to 1.0). Results shown are mean values from 3 experiments.
Proliferation effects of lenograstim (left column) and filgrastim (right column) on Kasumi-1, CTV-1, K562, and U266 cells at different concentrations (10, 50, and 100 ng/mL) after 72 h-incubation. The relative proliferation was expressed as percentage of unstimulated control cells (set to 100%).
Proliferation effects of lenograstim and filgrastim on Kasumi-1 cells according to incubation time at 10 ng/mL concentration of G-CSF. Both forms of G-CSF significantly stimulated the proliferation of
The differentiation effects of filgrastim (F) and lenograstim (L) on Kasumi-1 and CTV-1 cell lines and unstimulated control cells (C) after 14 d of incubation at 100 ng/mL. Both forms of G-CSF increased the percentage of CD11b positive cells in Kasumi-1 cells.
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Expression of G-CSFR in hematologic malignancies and solid tumors using real-time PCR. Among hematologic malignancies, Kasumi-1 and K562 expressed G-CSFR mRNA whereas CTV-1 and U266 did not. Among 38 solid tumor cell lines, 5 cell lines (13.1%) expressed G-CSFR mRNA. The G-CSFR expression of each cell type was normalized to GAPDH expression. The relative expressions were presented as relative ratios compared to gene expression in Kasumi-1 cells (set to 1.0). Results shown are mean values from 3 experiments.
|@|~(^,^)~|@|Proliferation effects of lenograstim (left column) and filgrastim (right column) on Kasumi-1, CTV-1, K562, and U266 cells at different concentrations (10, 50, and 100 ng/mL) after 72 h-incubation. The relative proliferation was expressed as percentage of unstimulated control cells (set to 100%).
|@|~(^,^)~|@|Proliferation effects of lenograstim and filgrastim on Kasumi-1 cells according to incubation time at 10 ng/mL concentration of G-CSF. Both forms of G-CSF significantly stimulated the proliferation of
The differentiation effects of filgrastim (F) and lenograstim (L) on Kasumi-1 and CTV-1 cell lines and unstimulated control cells (C) after 14 d of incubation at 100 ng/mL. Both forms of G-CSF increased the percentage of CD11b positive cells in Kasumi-1 cells.