Analysis of isoenzymes in normal and carcinogen-treated human endometrial stromal cells in culture

Karen Gray Nelson, Jill M. Siegfried, Gene P. Siegal, Jane L. Martin, David G. Kaufman

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

The isoenzyme patterns of lactate dehydrogenase (LDH), hexokinase, phosphofructokinase, and aldolase were investigated in cultured normal and carcinogen-treated human endometrial stromal cells. Both normal and carcinogen-treated cells had similar phosphofructokinase and aldolase isoenzymes. Distinctive changes in hexokinase and LDH isoenzyme patterns were found in the carcinogen-treated stromal cells. The LDH isoenzyme patterns of the carcinogen-treated stromal cells were shifted toward the muscle LDH forms. This is comparable to the alteration of LDH isoenzyme profiles observed in cell lines established from human uterine sarcomas. The two tissue culture media used affected the LDH isoenzyme patterns of endometrial stromal cells but differences between the LDH isoenzyme patterns of control and carcinogen-treated cells were detected regardless of the growth medium used. Total LDH activity was not significantly different in control and carcinogen-treated stromal cells. The hexokinase isoenzyme patterns expressed by the carcinogen-treated stromal cells were distinctly different from the normal hexokinase patterns. The treated stromal cells contained both hexokinase I and II, whereas the normal cells contained only hexokinase I. Hexokinase and LDH isoenzyme patterns may serve as markers with which to evaluate carcinogen-induced neoplastic changes in cultured endometrial stromal cells.

Original languageEnglish (US)
Pages (from-to)181-188
Number of pages8
JournalCarcinogenesis
Volume6
Issue number2
DOIs
StatePublished - Feb 1985
Externally publishedYes

Bibliographical note

Funding Information:
The authors acknowledge Dr Ming Tsao for assistance in isoenzyme analysis. We also thank Ms Amanda Wright for preparation of the manuscript. Supported by grant CA 31733 from the National Cancer Institute. KGN and JMS were supported by National Research Service Awards CA09156 and ES07017, respectively. GPS is a Junior Faculty Clinical Fellow (JFCF 739) of the American Cancer Society. DGK is the recipient of a Research Career Development Award (CA 00431) from the National Cancer Institute.

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