Effects of protein kinase Cδ and phospholipase C-γ1 on monocyte chemoattractant protein-1 expression in taxol-induced breast cancer cell death

Yoon Suk Kim, Hyoung Tae An, Jeonghan Kim, Je Sang Ko

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that plays an important role in immune cell migration. It has been reported that chemokines, including MCP-1, are involved in angiogenesis and metastasis. However, the exact role of chemokines in cancer development is still obscure. We investigated the involvement of MCP-1 in taxol-induced breast cancer cell death. The anti-cancer drug taxol induced MCF-7 breast cancer cell death. Treatment with taxol increased the mRNA expression level of MCP-1 in a dose- and time-dependent manner. Up-regulation of MCP-1 by taxol was augmented in cells treated with rottlerin, a specific inhibitor of protein kinase Cδ (PKCδ). In addition, taxol-induced MCP-1 expression was reduced by the ectopic expression of PKCδ in a dose-dependent manner, indicating that PKCδ plays a negative role in taxol-induced MCP-1 expression in MCF-7 cells. On the other hand, taxol-induced up-regulation of MCP-1 was reduced in cells treated with U73122, an inhibitor of phospholipase C (PLC), and ectopic expression of PLC-γ1 increased the expression of MCP-1 in taxol-treated MCF-7 cells, indicating that PLC-γ1 functions as a positive regulator in taxol-induced MCP-1 expression. These results indicate that MCP-1 is involved in taxol-induced breast cancer cell death and we propose that taxol induces up-regulation of MCP-1 by affecting both positive and negative regulatory signaling pathways.

Original languageEnglish
Pages (from-to)853-858
Number of pages6
JournalInternational Journal of Molecular Medicine
Volume24
Issue number6
DOIs
Publication statusPublished - 2009 Nov 11

Fingerprint

Chemokine CCL2
Type C Phospholipases
Paclitaxel
Protein Kinase C
Cell Death
Breast Neoplasms
Up-Regulation
MCF-7 Cells
Chemokines
CC Chemokines
Cell Movement
Neoplasms

Keywords

  • Breast cancer
  • MCP-1
  • Protein kinase Cδ phospholipase C
  • Signal transduction
  • Taxol

ASJC Scopus subject areas

  • Genetics

Cite this

Effects of protein kinase Cδ and phospholipase C-γ1 on monocyte chemoattractant protein-1 expression in taxol-induced breast cancer cell death. / Kim, Yoon Suk; An, Hyoung Tae; Kim, Jeonghan; Ko, Je Sang.

In: International Journal of Molecular Medicine, Vol. 24, No. 6, 11.11.2009, p. 853-858.

Research output: Contribution to journalArticle

@article{1b841345ff8c4ba38197331724168734,
title = "Effects of protein kinase Cδ and phospholipase C-γ1 on monocyte chemoattractant protein-1 expression in taxol-induced breast cancer cell death",
abstract = "Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that plays an important role in immune cell migration. It has been reported that chemokines, including MCP-1, are involved in angiogenesis and metastasis. However, the exact role of chemokines in cancer development is still obscure. We investigated the involvement of MCP-1 in taxol-induced breast cancer cell death. The anti-cancer drug taxol induced MCF-7 breast cancer cell death. Treatment with taxol increased the mRNA expression level of MCP-1 in a dose- and time-dependent manner. Up-regulation of MCP-1 by taxol was augmented in cells treated with rottlerin, a specific inhibitor of protein kinase Cδ (PKCδ). In addition, taxol-induced MCP-1 expression was reduced by the ectopic expression of PKCδ in a dose-dependent manner, indicating that PKCδ plays a negative role in taxol-induced MCP-1 expression in MCF-7 cells. On the other hand, taxol-induced up-regulation of MCP-1 was reduced in cells treated with U73122, an inhibitor of phospholipase C (PLC), and ectopic expression of PLC-γ1 increased the expression of MCP-1 in taxol-treated MCF-7 cells, indicating that PLC-γ1 functions as a positive regulator in taxol-induced MCP-1 expression. These results indicate that MCP-1 is involved in taxol-induced breast cancer cell death and we propose that taxol induces up-regulation of MCP-1 by affecting both positive and negative regulatory signaling pathways.",
keywords = "Breast cancer, MCP-1, Protein kinase Cδ phospholipase C, Signal transduction, Taxol",
author = "Kim, {Yoon Suk} and An, {Hyoung Tae} and Jeonghan Kim and Ko, {Je Sang}",
year = "2009",
month = "11",
day = "11",
doi = "10.3892/ijmm_00000303",
language = "English",
volume = "24",
pages = "853--858",
journal = "International Journal of Molecular Medicine",
issn = "1107-3756",
publisher = "Spandidos Publications",
number = "6",

}

TY - JOUR

T1 - Effects of protein kinase Cδ and phospholipase C-γ1 on monocyte chemoattractant protein-1 expression in taxol-induced breast cancer cell death

AU - Kim, Yoon Suk

AU - An, Hyoung Tae

AU - Kim, Jeonghan

AU - Ko, Je Sang

PY - 2009/11/11

Y1 - 2009/11/11

N2 - Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that plays an important role in immune cell migration. It has been reported that chemokines, including MCP-1, are involved in angiogenesis and metastasis. However, the exact role of chemokines in cancer development is still obscure. We investigated the involvement of MCP-1 in taxol-induced breast cancer cell death. The anti-cancer drug taxol induced MCF-7 breast cancer cell death. Treatment with taxol increased the mRNA expression level of MCP-1 in a dose- and time-dependent manner. Up-regulation of MCP-1 by taxol was augmented in cells treated with rottlerin, a specific inhibitor of protein kinase Cδ (PKCδ). In addition, taxol-induced MCP-1 expression was reduced by the ectopic expression of PKCδ in a dose-dependent manner, indicating that PKCδ plays a negative role in taxol-induced MCP-1 expression in MCF-7 cells. On the other hand, taxol-induced up-regulation of MCP-1 was reduced in cells treated with U73122, an inhibitor of phospholipase C (PLC), and ectopic expression of PLC-γ1 increased the expression of MCP-1 in taxol-treated MCF-7 cells, indicating that PLC-γ1 functions as a positive regulator in taxol-induced MCP-1 expression. These results indicate that MCP-1 is involved in taxol-induced breast cancer cell death and we propose that taxol induces up-regulation of MCP-1 by affecting both positive and negative regulatory signaling pathways.

AB - Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that plays an important role in immune cell migration. It has been reported that chemokines, including MCP-1, are involved in angiogenesis and metastasis. However, the exact role of chemokines in cancer development is still obscure. We investigated the involvement of MCP-1 in taxol-induced breast cancer cell death. The anti-cancer drug taxol induced MCF-7 breast cancer cell death. Treatment with taxol increased the mRNA expression level of MCP-1 in a dose- and time-dependent manner. Up-regulation of MCP-1 by taxol was augmented in cells treated with rottlerin, a specific inhibitor of protein kinase Cδ (PKCδ). In addition, taxol-induced MCP-1 expression was reduced by the ectopic expression of PKCδ in a dose-dependent manner, indicating that PKCδ plays a negative role in taxol-induced MCP-1 expression in MCF-7 cells. On the other hand, taxol-induced up-regulation of MCP-1 was reduced in cells treated with U73122, an inhibitor of phospholipase C (PLC), and ectopic expression of PLC-γ1 increased the expression of MCP-1 in taxol-treated MCF-7 cells, indicating that PLC-γ1 functions as a positive regulator in taxol-induced MCP-1 expression. These results indicate that MCP-1 is involved in taxol-induced breast cancer cell death and we propose that taxol induces up-regulation of MCP-1 by affecting both positive and negative regulatory signaling pathways.

KW - Breast cancer

KW - MCP-1

KW - Protein kinase Cδ phospholipase C

KW - Signal transduction

KW - Taxol

UR - http://www.scopus.com/inward/record.url?scp=70350776994&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70350776994&partnerID=8YFLogxK

U2 - 10.3892/ijmm_00000303

DO - 10.3892/ijmm_00000303

M3 - Article

VL - 24

SP - 853

EP - 858

JO - International Journal of Molecular Medicine

JF - International Journal of Molecular Medicine

SN - 1107-3756

IS - 6

ER -