Expression of c-Myc in glucocorticoid-treated fibroblastic cells

Gloria H. Frost, Kunsoo Rhee, Tianlin Ma, E Aubrey Thompson

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Glucocorticoids inhibit proliferation of L929 fibroblastic cells in culture. Inhibition of proliferation is reversible and is not associated with changes in the plating efficiency of the cells. Flow cytometric analysis indicates that glucocorticoid-treated cells exhibit a decrease in the percentage of cells with DNA content >2N. Thymidine kinase expression is inhibited as cells with 2N DNA content accumulate. These observations indicate that glucocorticoids arrest proliferation of L929 cells in the G1 phase of the cell cycle. The abundance of c-Myc mRNA does not decrease in glucocorticoid-treated cells, and c-Myc protein content in dexamethasone-treated cells is approximately the same as that detected in mid-log phase cells. Nuclear run-on transcription of c-Myc is not inhibited by glucocorticoids. These observations indicate that glucocorticoid regulation of fibroblastic cell proliferation does not involve inhibition of c-Myc transcription. Although regulation of c-Myc expression is central to the mechanism whereby glucocorticoids regulate proliferation of lymphoid cells, it is clear that different mechanisms must be involved in glucocorticoid regulation of fibroblastic cell proliferation.

Original languageEnglish (US)
Pages (from-to)109-119
Number of pages11
JournalJournal of Steroid Biochemistry and Molecular Biology
Volume50
Issue number3-4
DOIs
StatePublished - 1994
Externally publishedYes

Fingerprint

Glucocorticoids
Cells
Cell Proliferation
Cell proliferation
Transcription
Proto-Oncogene Proteins c-myc
Thymidine Kinase
DNA
G1 Phase
Plating
Dexamethasone
Cell Cycle
Cell Culture Techniques
Lymphocytes
Messenger RNA

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Expression of c-Myc in glucocorticoid-treated fibroblastic cells. / Frost, Gloria H.; Rhee, Kunsoo; Ma, Tianlin; Thompson, E Aubrey.

In: Journal of Steroid Biochemistry and Molecular Biology, Vol. 50, No. 3-4, 1994, p. 109-119.

Research output: Contribution to journalArticle

Frost, Gloria H. ; Rhee, Kunsoo ; Ma, Tianlin ; Thompson, E Aubrey. / Expression of c-Myc in glucocorticoid-treated fibroblastic cells. In: Journal of Steroid Biochemistry and Molecular Biology. 1994 ; Vol. 50, No. 3-4. pp. 109-119.
@article{f6ea78c418d14a6f95d98e037d438460,
title = "Expression of c-Myc in glucocorticoid-treated fibroblastic cells",
abstract = "Glucocorticoids inhibit proliferation of L929 fibroblastic cells in culture. Inhibition of proliferation is reversible and is not associated with changes in the plating efficiency of the cells. Flow cytometric analysis indicates that glucocorticoid-treated cells exhibit a decrease in the percentage of cells with DNA content >2N. Thymidine kinase expression is inhibited as cells with 2N DNA content accumulate. These observations indicate that glucocorticoids arrest proliferation of L929 cells in the G1 phase of the cell cycle. The abundance of c-Myc mRNA does not decrease in glucocorticoid-treated cells, and c-Myc protein content in dexamethasone-treated cells is approximately the same as that detected in mid-log phase cells. Nuclear run-on transcription of c-Myc is not inhibited by glucocorticoids. These observations indicate that glucocorticoid regulation of fibroblastic cell proliferation does not involve inhibition of c-Myc transcription. Although regulation of c-Myc expression is central to the mechanism whereby glucocorticoids regulate proliferation of lymphoid cells, it is clear that different mechanisms must be involved in glucocorticoid regulation of fibroblastic cell proliferation.",
author = "Frost, {Gloria H.} and Kunsoo Rhee and Tianlin Ma and Thompson, {E Aubrey}",
year = "1994",
doi = "10.1016/0960-0760(94)90017-5",
language = "English (US)",
volume = "50",
pages = "109--119",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
issn = "0960-0760",
publisher = "Elsevier Limited",
number = "3-4",

}

TY - JOUR

T1 - Expression of c-Myc in glucocorticoid-treated fibroblastic cells

AU - Frost, Gloria H.

AU - Rhee, Kunsoo

AU - Ma, Tianlin

AU - Thompson, E Aubrey

PY - 1994

Y1 - 1994

N2 - Glucocorticoids inhibit proliferation of L929 fibroblastic cells in culture. Inhibition of proliferation is reversible and is not associated with changes in the plating efficiency of the cells. Flow cytometric analysis indicates that glucocorticoid-treated cells exhibit a decrease in the percentage of cells with DNA content >2N. Thymidine kinase expression is inhibited as cells with 2N DNA content accumulate. These observations indicate that glucocorticoids arrest proliferation of L929 cells in the G1 phase of the cell cycle. The abundance of c-Myc mRNA does not decrease in glucocorticoid-treated cells, and c-Myc protein content in dexamethasone-treated cells is approximately the same as that detected in mid-log phase cells. Nuclear run-on transcription of c-Myc is not inhibited by glucocorticoids. These observations indicate that glucocorticoid regulation of fibroblastic cell proliferation does not involve inhibition of c-Myc transcription. Although regulation of c-Myc expression is central to the mechanism whereby glucocorticoids regulate proliferation of lymphoid cells, it is clear that different mechanisms must be involved in glucocorticoid regulation of fibroblastic cell proliferation.

AB - Glucocorticoids inhibit proliferation of L929 fibroblastic cells in culture. Inhibition of proliferation is reversible and is not associated with changes in the plating efficiency of the cells. Flow cytometric analysis indicates that glucocorticoid-treated cells exhibit a decrease in the percentage of cells with DNA content >2N. Thymidine kinase expression is inhibited as cells with 2N DNA content accumulate. These observations indicate that glucocorticoids arrest proliferation of L929 cells in the G1 phase of the cell cycle. The abundance of c-Myc mRNA does not decrease in glucocorticoid-treated cells, and c-Myc protein content in dexamethasone-treated cells is approximately the same as that detected in mid-log phase cells. Nuclear run-on transcription of c-Myc is not inhibited by glucocorticoids. These observations indicate that glucocorticoid regulation of fibroblastic cell proliferation does not involve inhibition of c-Myc transcription. Although regulation of c-Myc expression is central to the mechanism whereby glucocorticoids regulate proliferation of lymphoid cells, it is clear that different mechanisms must be involved in glucocorticoid regulation of fibroblastic cell proliferation.

UR - http://www.scopus.com/inward/record.url?scp=0028122760&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028122760&partnerID=8YFLogxK

U2 - 10.1016/0960-0760(94)90017-5

DO - 10.1016/0960-0760(94)90017-5

M3 - Article

C2 - 8049139

AN - SCOPUS:0028122760

VL - 50

SP - 109

EP - 119

JO - Journal of Steroid Biochemistry and Molecular Biology

JF - Journal of Steroid Biochemistry and Molecular Biology

SN - 0960-0760

IS - 3-4

ER -