Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway

Hong Nu Yu; Young Rae Lee; Eun Mi Noh; Kyung Sun Lee; Eun Kyung Song; Myung Kwan Han; Yong Chul Lee; Chang Yeol Yim; Jinny Park; Byeong Soo Kim; Sung Ho Lee; Seung Jin Lee; Jong Suk Kim

doi:10.1007/s12185-008-0037-z

Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway

Hong Nu Yu, Young Rae Lee, Eun Mi Noh, Kyung Sun Lee, Eun Kyung Song, Myung Kwan Han, Yong Chul Lee, Chang Yeol Yim, Jinny Park, Byeong Soo Kim, Sung Ho Lee, Seung Jin Lee, Jong Suk Kim

Department of Pharmaceutical Sciences

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

21 Scopus citations

Abstract

The differentiation of promyelocytic leukemic cells into mature cells is the major strategy for drug-based treatment of leukemia. Higher efficient methods to differentiate promyelocytic leukemic cells have been developed using various differentiation inducers including interferon-α, interleukin-4, tumor necrosis factor-α (TNF-α), and dimethyl sulfoxide (DMSO) as a single agent or in combination with each other. Here, we show that a combination of TNF-α with DMSO shows a synergic effect on HL-60 cell differentiation through the activation of ERK pathway. TNF-α enhanced CD11b expression and percent of cell population in the G₁ phase induced by DMSO, which are hallmarks for HL-60 cell differentiation. Inhibition of ERK pathway abolished the synergic effect of TNF-α in combination with DMSO on HL-60 differentiation, but the inhibition NF-κB pathway did not. These results suggest that TNF-α synergistically increases DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK-signaling pathway.

Original language	English
Pages (from-to)	189-194
Number of pages	6
Journal	International Journal of Hematology
Volume	87
Issue number	2
DOIs	https://doi.org/10.1007/s12185-008-0037-z
State	Published - Mar 2008

Bibliographical note

Funding Information:
Acknowledgments This work was supported by grants of the Korea Science and Engineering Foundation (nos. R01-2002-000-00493-0, R11-2002-100-02007-0, and M10528010003-05N2801-00310) and the grant of Post Doc. Program, Chonbuk National University (K.-S. Lee).

Keywords

DMSO
Leukemic cell differentiation
MAPK
NF-κB
TNF-α

Access to Document

10.1007/s12185-008-0037-z

Cite this

Yu, H. N., Lee, Y. R., Noh, E. M., Lee, K. S., Song, E. K., Han, M. K., Lee, Y. C., Yim, C. Y., Park, J., Kim, B. S., Lee, S. H., Lee, S. J., & Kim, J. S. (2008). Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway. International Journal of Hematology, 87(2), 189-194. https://doi.org/10.1007/s12185-008-0037-z

@article{13612a4baf5d45389318787b6d8bc32d,

title = "Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway",

abstract = "The differentiation of promyelocytic leukemic cells into mature cells is the major strategy for drug-based treatment of leukemia. Higher efficient methods to differentiate promyelocytic leukemic cells have been developed using various differentiation inducers including interferon-α, interleukin-4, tumor necrosis factor-α (TNF-α), and dimethyl sulfoxide (DMSO) as a single agent or in combination with each other. Here, we show that a combination of TNF-α with DMSO shows a synergic effect on HL-60 cell differentiation through the activation of ERK pathway. TNF-α enhanced CD11b expression and percent of cell population in the G1 phase induced by DMSO, which are hallmarks for HL-60 cell differentiation. Inhibition of ERK pathway abolished the synergic effect of TNF-α in combination with DMSO on HL-60 differentiation, but the inhibition NF-κB pathway did not. These results suggest that TNF-α synergistically increases DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK-signaling pathway.",

keywords = "DMSO, Leukemic cell differentiation, MAPK, NF-κB, TNF-α",

author = "Yu, {Hong Nu} and Lee, {Young Rae} and Noh, {Eun Mi} and Lee, {Kyung Sun} and Song, {Eun Kyung} and Han, {Myung Kwan} and Lee, {Yong Chul} and Yim, {Chang Yeol} and Jinny Park and Kim, {Byeong Soo} and Lee, {Sung Ho} and Lee, {Seung Jin} and Kim, {Jong Suk}",

note = "Funding Information: Acknowledgments This work was supported by grants of the Korea Science and Engineering Foundation (nos. R01-2002-000-00493-0, R11-2002-100-02007-0, and M10528010003-05N2801-00310) and the grant of Post Doc. Program, Chonbuk National University (K.-S. Lee).",

year = "2008",

month = mar,

doi = "10.1007/s12185-008-0037-z",

language = "English",

volume = "87",

pages = "189--194",

journal = "International Journal of Hematology",

issn = "0925-5710",

publisher = "Springer",

number = "2",

}

TY - JOUR

T1 - Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway

AU - Yu, Hong Nu

AU - Lee, Young Rae

AU - Noh, Eun Mi

AU - Lee, Kyung Sun

AU - Song, Eun Kyung

AU - Han, Myung Kwan

AU - Lee, Yong Chul

AU - Yim, Chang Yeol

AU - Park, Jinny

AU - Kim, Byeong Soo

AU - Lee, Sung Ho

AU - Lee, Seung Jin

AU - Kim, Jong Suk

N1 - Funding Information: Acknowledgments This work was supported by grants of the Korea Science and Engineering Foundation (nos. R01-2002-000-00493-0, R11-2002-100-02007-0, and M10528010003-05N2801-00310) and the grant of Post Doc. Program, Chonbuk National University (K.-S. Lee).

PY - 2008/3

Y1 - 2008/3

N2 - The differentiation of promyelocytic leukemic cells into mature cells is the major strategy for drug-based treatment of leukemia. Higher efficient methods to differentiate promyelocytic leukemic cells have been developed using various differentiation inducers including interferon-α, interleukin-4, tumor necrosis factor-α (TNF-α), and dimethyl sulfoxide (DMSO) as a single agent or in combination with each other. Here, we show that a combination of TNF-α with DMSO shows a synergic effect on HL-60 cell differentiation through the activation of ERK pathway. TNF-α enhanced CD11b expression and percent of cell population in the G1 phase induced by DMSO, which are hallmarks for HL-60 cell differentiation. Inhibition of ERK pathway abolished the synergic effect of TNF-α in combination with DMSO on HL-60 differentiation, but the inhibition NF-κB pathway did not. These results suggest that TNF-α synergistically increases DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK-signaling pathway.

AB - The differentiation of promyelocytic leukemic cells into mature cells is the major strategy for drug-based treatment of leukemia. Higher efficient methods to differentiate promyelocytic leukemic cells have been developed using various differentiation inducers including interferon-α, interleukin-4, tumor necrosis factor-α (TNF-α), and dimethyl sulfoxide (DMSO) as a single agent or in combination with each other. Here, we show that a combination of TNF-α with DMSO shows a synergic effect on HL-60 cell differentiation through the activation of ERK pathway. TNF-α enhanced CD11b expression and percent of cell population in the G1 phase induced by DMSO, which are hallmarks for HL-60 cell differentiation. Inhibition of ERK pathway abolished the synergic effect of TNF-α in combination with DMSO on HL-60 differentiation, but the inhibition NF-κB pathway did not. These results suggest that TNF-α synergistically increases DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK-signaling pathway.

KW - DMSO

KW - Leukemic cell differentiation

KW - MAPK

KW - NF-κB

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=42049115249&partnerID=8YFLogxK

U2 - 10.1007/s12185-008-0037-z

DO - 10.1007/s12185-008-0037-z

M3 - Article

C2 - 18256785

AN - SCOPUS:42049115249

SN - 0925-5710

VL - 87

SP - 189

EP - 194

JO - International Journal of Hematology

JF - International Journal of Hematology

IS - 2

ER -

Tumor necrosis factor-α enhances DMSO-induced differentiation of HL-60 cells through the activation of ERK/MAPK pathway

Abstract

Bibliographical note

Keywords

Access to Document

Fingerprint

Cite this