Download adenosine deaminase activity in estrogen receptor positive and

Medical Journal of the
Islamic Republic of Iran
Volume 19
Number I
Spring 1384
May 2005
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ADENOSINE DEAMINASE ACTIVITY IN ESTROGEN
RECEPTOR POSITIVE AND NEGATIVE HUMAN
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BREAST CANCER CELL LINES
MOHAMMAD HASHEMI,"1 FATEMEH KARAMI TEHRANI/ SAEID
GHAVAMI, 1 AND MAJID SIRATI SABET.3
From the IDept. of Clinical Biochemistry, School of Medicine, Zahedan Medical University, Zahedan, iran,
the 2Cancer Research Lab, Dept. of Clinical Biochemistry, School of Medical Sciences, Tarbiat Modarres
University, Tehran, Iran, and the 3Dept. olClinical Biochemistry, School of Medicine, Qazvin Medical
University, Qazvin, Iran.
ABSTRACT
Background: The aims of this study were to assay the activity of adenosine deami­
nase (ADA) in estrogen receptor positive (MCF-7) and negative (MDA-MB468)
breast cancer cell lines.
Methods: MDA-MB468 and MCF-7 breast cancer cell lines were cultured in
complete medium, striped serum with and without 0.0 111M diethylstilbestrol (DES),
complete medium in the presence and absence of 111M tamoxifen for 20 hr. Adenosine
deaminase activity was determined using the colorimetric method described by Guisti
and Galanti.
Results: It was found that the activity of enzyme in estrogen receptor positive
(ER+) cell line (MCF-7) was significantly higher than that of estrogen receptor negative
breast cancer cell line (MDA-MB468). ADA activity in MCF-7 cells cultured in the
presence of tamoxifen or charcoal-striped serum was significantly lower than that of
control. Furthermore addition of diethylstilbestrol (DES) to the striped serum increased
the value of ADA activity to that of control.
Unlike MCF-7 cells, the activity of ADA in MDA-MB468 cells remained un­
changed upon treatment with tamoxifen or striped serum.
Conclusion: These findings suggest estrogen responsiveness of ADA expression
in MCF-7 cells.
MJIRI, Vol. 19, No.1, 53-56, 2005.
Keywords: Adenosine deaminase, breast cancer cell lines, estrogen receptor.
INTRODUCTION
loenzyme that catalyzes the deamination of adenosine
and deoxyadenosine to inosine and deoxyinosine, re­
Adenosine deaminase (ADA,
"Corresponding author:
E.C.3.S.4.4) is a metal-
Mohammad Hashemi, Ph.D., Dept. of
Clinical Biochemistry, Zahedan Medical University, Zahedan, Iran.
Tel.:
09173640366
spectively. I Due to the irreversibility of the reaction cata­
lyzed by ADA, this enzyme reaction seems to be one of
the rate-limiting steps in adenosine degradation. ADA is
present in virtually all human tissues, but the highest
e-mail: mhdha [email protected]
/53
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ADAActivity in ER Positive and Negative Breast Cancer
ity when compared to that of control, in contrast to the
cer cells in tissue culture. Cancer Res 43: 4681-4690, 1983.
reduce enzyme activity, although not at the same magni­
11. Aitken SC, Lippman ME, Kasid A, Schoenberg DR: Rela ­
tude as that observed for stripped serum. Furthermore,
tionship between the expression of e strogen-regulated genes
addition of DES, a potent synthetic estrogen, to the
and estrogen-stimulated proliferation of MCF-7 m ammary
stripped culture media stimulated ADA expression and
tumor cells. Cancer Res 45: 2608-2615,1985
restored the activity. MDA-MB468 cells, however, ex­
hibited no changes in ADA activity upon treatment with
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pyrimidine synthesis and utilization in human b r e ast can­
report of Xie et al,15 tamoxifen alone did significantly
12.
Aitken SC, Lippman ME: Effect of est r o g e n and
antiestrogens on growth-regulatory enzymes in h uma n
tamoxifen of removing estrogen from the media. These
breast cancer cells in tissue culture. Cancer Res 45: 1611-
findings suggest E2 responsiveness of ADA expression
1620, 1985.
in MCF-7 cells. In the MDA-MB468 cell line, the ADA
13. Cowan K, Levine R, Aitken S, G o l dsmith M, Douglass E,
gene is not an E2 target gene and there must be other
Clendeninn N, Nienhuis A, Lippman ME: Dihydr ofolate
nuclear transcription factors to induce ADA expression.
reductase gene amplification and possible rearrangement in
It has been demonstrated that tamoxifen induces a
estrogen-responsive methotrexate resistant human breast
significant apoptosis in the MCF-7 cell line.23 One pos­
sible mechanism might be through the inhibition of ADA
cancer cells. J BioI Chern 257: 15079-15086,1982.
14. Kasid A, Davidson NE, Gelmann EP, Lippman ME: Tran­
and subsequent accumulation of toxic adenosine and
scriptional control of thymidine kinase gene expression by
deoxyadenosine that causes inhibition of ribonucleotide
estrogens and anti estrogens in MCF-7 human breast cancer
reductase and also inactivation of s-adenosyl homocys­
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cells. J BioI Chern 261: 5562-5567,1986.
15. Xie W, Duan R, Safe S: Estrogen induces adenosine deami­
nase gene expression in MCF-7 human breast cancer cells:
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