Regulation of protein kinase C δ by estrogen in the MCF-7 human breast cancer cell line

Malathy Shanmugam; Nancy L. Krett; Evelyn T. Maizels; Richard E. Cutler; Carl A. Peters; Leia M. Smith; Michelle L. O'Brien; Ok Kyong Park-Sarge; Steven T. Rosen; Mary Hunzicker-Dunn

doi:10.1016/S0303-7207(98)00229-9

Regulation of protein kinase C δ by estrogen in the MCF-7 human breast cancer cell line

Malathy Shanmugam, Nancy L. Krett, Evelyn T. Maizels, Richard E. Cutler, Carl A. Peters, Leia M. Smith, Michelle L. O'Brien, Ok Kyong Park-Sarge, Steven T. Rosen, Mary Hunzicker-Dunn

Physiology

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

45 Scopus citations

Abstract

We have previously shown that estrogen up-regulates expression of protein kinase C (PKC) δ in the rat and rabbit corpus luteum as well as in luteinized rat granulosa primary cell cultures. To determine whether a similar regulation of the PKC δ isoform by estrogen occurred in another estrogen responsive system, we investigated the estrogen receptor positive MCF-7 human breast cancer cells. In a characterization of PKC isoforms in MCF-7 cells we determined that PKC δ was the predominant PKC isoform. However in contrast to the effect of estrogen on PKC δ expression in ovarian cells, estrogen treatment of MCF-7 cells resulted in a significant decrease in PKC δ protein and mRNA expression in a time and dose dependent manner. Treatment of MCF-7 cells with 10^-10-10^-8 M estrogen for 7 days down- regulated specifically PKC δ mRNA and protein while expression of other PKC isoforms was unchanged. The opposite regulation of PKC δ expression in ovarian and breast cancer cells prompted us to evaluate the type of estrogen receptor present in both cell types. Results showed that luteinized rat granulosa cells expressed predominantly estrogen receptor β while the MCF-7 cells expressed predominantly estrogen receptor α and barely detectable levels of estrogen receptor β. These results suggest that the differential ability of estrogen to regulate PKC δ expression could potentially be a result of differential signaling through the two estrogen receptor subtypes.

Original language	English
Pages (from-to)	109-118
Number of pages	10
Journal	Molecular and Cellular Endocrinology
Volume	148
Issue number	1-2
DOIs	https://doi.org/10.1016/S0303-7207(98)00229-9
State	Published - Feb 25 1999

Bibliographical note

Funding Information:
We gratefully acknowledge the gifts of PKC antisera from Drs S. Ohno and K. Mizuno, Yokohama City University School of Medicine, Japan; Dr K. Leach (Upjohn Co., MI); Dr D.K. Ways (East Carolina University School of Medicine, North Carolina). We would also like to thank Dr P.J. Parker (Imperial Cancer Research Fund, London) for the PKC δ cDNA and Dr Craig Jordan for providing us with ICI 164384. This work was supported by the Breast and Cervical Cancer Research Fund, Illinois Department of Public Health B21N (MHD), P30 CA60553 (SR), and NIH HD30719 (O-KP-S).

Keywords

Breast cancer
Estrogen
PKC δ
Signal transduction

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Endocrinology

UN SDGs

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

Access to Document

10.1016/S0303-7207(98)00229-9

Cite this

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title = "Regulation of protein kinase C δ by estrogen in the MCF-7 human breast cancer cell line",

abstract = "We have previously shown that estrogen up-regulates expression of protein kinase C (PKC) δ in the rat and rabbit corpus luteum as well as in luteinized rat granulosa primary cell cultures. To determine whether a similar regulation of the PKC δ isoform by estrogen occurred in another estrogen responsive system, we investigated the estrogen receptor positive MCF-7 human breast cancer cells. In a characterization of PKC isoforms in MCF-7 cells we determined that PKC δ was the predominant PKC isoform. However in contrast to the effect of estrogen on PKC δ expression in ovarian cells, estrogen treatment of MCF-7 cells resulted in a significant decrease in PKC δ protein and mRNA expression in a time and dose dependent manner. Treatment of MCF-7 cells with 10-10-10-8 M estrogen for 7 days down- regulated specifically PKC δ mRNA and protein while expression of other PKC isoforms was unchanged. The opposite regulation of PKC δ expression in ovarian and breast cancer cells prompted us to evaluate the type of estrogen receptor present in both cell types. Results showed that luteinized rat granulosa cells expressed predominantly estrogen receptor β while the MCF-7 cells expressed predominantly estrogen receptor α and barely detectable levels of estrogen receptor β. These results suggest that the differential ability of estrogen to regulate PKC δ expression could potentially be a result of differential signaling through the two estrogen receptor subtypes.",

keywords = "Breast cancer, Estrogen, PKC δ, Signal transduction",

author = "Malathy Shanmugam and Krett, {Nancy L.} and Maizels, {Evelyn T.} and Cutler, {Richard E.} and Peters, {Carl A.} and Smith, {Leia M.} and O'Brien, {Michelle L.} and Park-Sarge, {Ok Kyong} and Rosen, {Steven T.} and Mary Hunzicker-Dunn",

note = "Funding Information: We gratefully acknowledge the gifts of PKC antisera from Drs S. Ohno and K. Mizuno, Yokohama City University School of Medicine, Japan; Dr K. Leach (Upjohn Co., MI); Dr D.K. Ways (East Carolina University School of Medicine, North Carolina). We would also like to thank Dr P.J. Parker (Imperial Cancer Research Fund, London) for the PKC δ cDNA and Dr Craig Jordan for providing us with ICI 164384. This work was supported by the Breast and Cervical Cancer Research Fund, Illinois Department of Public Health B21N (MHD), P30 CA60553 (SR), and NIH HD30719 (O-KP-S).",

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AU - Krett, Nancy L.

AU - Maizels, Evelyn T.

AU - Cutler, Richard E.

AU - Peters, Carl A.

AU - Smith, Leia M.

AU - O'Brien, Michelle L.

AU - Park-Sarge, Ok Kyong

AU - Rosen, Steven T.

AU - Hunzicker-Dunn, Mary

N1 - Funding Information: We gratefully acknowledge the gifts of PKC antisera from Drs S. Ohno and K. Mizuno, Yokohama City University School of Medicine, Japan; Dr K. Leach (Upjohn Co., MI); Dr D.K. Ways (East Carolina University School of Medicine, North Carolina). We would also like to thank Dr P.J. Parker (Imperial Cancer Research Fund, London) for the PKC δ cDNA and Dr Craig Jordan for providing us with ICI 164384. This work was supported by the Breast and Cervical Cancer Research Fund, Illinois Department of Public Health B21N (MHD), P30 CA60553 (SR), and NIH HD30719 (O-KP-S).

PY - 1999/2/25

Y1 - 1999/2/25

N2 - We have previously shown that estrogen up-regulates expression of protein kinase C (PKC) δ in the rat and rabbit corpus luteum as well as in luteinized rat granulosa primary cell cultures. To determine whether a similar regulation of the PKC δ isoform by estrogen occurred in another estrogen responsive system, we investigated the estrogen receptor positive MCF-7 human breast cancer cells. In a characterization of PKC isoforms in MCF-7 cells we determined that PKC δ was the predominant PKC isoform. However in contrast to the effect of estrogen on PKC δ expression in ovarian cells, estrogen treatment of MCF-7 cells resulted in a significant decrease in PKC δ protein and mRNA expression in a time and dose dependent manner. Treatment of MCF-7 cells with 10-10-10-8 M estrogen for 7 days down- regulated specifically PKC δ mRNA and protein while expression of other PKC isoforms was unchanged. The opposite regulation of PKC δ expression in ovarian and breast cancer cells prompted us to evaluate the type of estrogen receptor present in both cell types. Results showed that luteinized rat granulosa cells expressed predominantly estrogen receptor β while the MCF-7 cells expressed predominantly estrogen receptor α and barely detectable levels of estrogen receptor β. These results suggest that the differential ability of estrogen to regulate PKC δ expression could potentially be a result of differential signaling through the two estrogen receptor subtypes.

AB - We have previously shown that estrogen up-regulates expression of protein kinase C (PKC) δ in the rat and rabbit corpus luteum as well as in luteinized rat granulosa primary cell cultures. To determine whether a similar regulation of the PKC δ isoform by estrogen occurred in another estrogen responsive system, we investigated the estrogen receptor positive MCF-7 human breast cancer cells. In a characterization of PKC isoforms in MCF-7 cells we determined that PKC δ was the predominant PKC isoform. However in contrast to the effect of estrogen on PKC δ expression in ovarian cells, estrogen treatment of MCF-7 cells resulted in a significant decrease in PKC δ protein and mRNA expression in a time and dose dependent manner. Treatment of MCF-7 cells with 10-10-10-8 M estrogen for 7 days down- regulated specifically PKC δ mRNA and protein while expression of other PKC isoforms was unchanged. The opposite regulation of PKC δ expression in ovarian and breast cancer cells prompted us to evaluate the type of estrogen receptor present in both cell types. Results showed that luteinized rat granulosa cells expressed predominantly estrogen receptor β while the MCF-7 cells expressed predominantly estrogen receptor α and barely detectable levels of estrogen receptor β. These results suggest that the differential ability of estrogen to regulate PKC δ expression could potentially be a result of differential signaling through the two estrogen receptor subtypes.

KW - Breast cancer

KW - Estrogen

KW - PKC δ

KW - Signal transduction

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JO - Molecular and Cellular Endocrinology

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IS - 1-2

ER -

Regulation of protein kinase C δ by estrogen in the MCF-7 human breast cancer cell line

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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