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1 in the expression of early growth response 1 gene in rat 3Y1 fibroblasts
* Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, Korea 705–717;
Department of Microbiology, Kyungpook National University, Daegu, Korea 702–701;
Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea 138–736;
Department of Biology, Daejin University, Pochon-gun, Kyeonggido, Korea 487–800;
|| Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul, Korea 137–701;
¶ Chonnam National University Research Institute of Medical Sciences, Kwangju, Korea 501–746;
Department of Life Science, Pohang University of Science and Technology, Pohang, Korea 790–784;
Green Cross Institute of Medical Genetics, Seoul, Korea 135–260;
Department of Psychiatry, Clinical Research Institute, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea 151-742; and
** Department of Biochemistry, University of Ulsan College of Medicine, Seoul, Korea 138–736,
1Correspondence: Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, 317–1, Daemyung-Dong, Nam-Gu, Daegu 705–717, South Korea. E-mail: younglee{at}med.yu.ac.kr
The early growth response 1 (Egr-1) gene product is a transcription factor that functions as an oikis factor. Loss of Egr-1 expression is closely associated with tumor formation. Phospholipase C
1 (PLC1) is overexpressed in some tumors, and its overexpression causes anchorage-independent growth. Here we report that overexpression of PLC1 and SH2-SH3 domain of PLC1 decreased induction of Egr-1 and the Egr-1-regulated genes TSP-1 and PAI-1. Results from the nuclear run-on assay and transfection experiment with the proximal 455 base pair region of the Egr-1 promoter (-454 to +1) showed that Egr-1 transcriptional activity was suppressed in PLC1–3Y1 cells whereas decay of Egr-1 mRNA was similar in both cell lines. Serum response element- and ternary complex factor Elk-1-mediated transcriptional activation of the reporter gene in response to EGF were also inhibited in PLC1–3Y1 cells. Pretreatment with the protein synthesis inhibitor cycloheximide (CHX) partially abrogated the serum-induced suppression of Egr-1 transcription in PLC1–3Y1 cells, suggesting that a CHX-sensitive factor(s) is involved in the suppression of Egr-1 transcription in PLC1–3Y1 cells. Our results demonstrated that overexpression of PLC1 functions as a negative modulator of the tumor suppressor Egr-1 gene expression, possibly through inhibition of Elk-1-dependent transcriptional activity.—Shin, S. Y., Ko, J., Chang, J.-S., Min, D. S., Choi, C., Bae, S. S., Kim, M. J., Hyun, D. S., Kim, J.-H., Han, M. Y., Kim, Y.-H., Kim, Y. S., Na, D. S., Suh, P.-G., Lee, Y. H. Negative regulatory role of overexpression of PLC1 in the expression of early growth response 1 gene in rat 3Y1 fibroblasts.
Key Words: Egr-1 • tumor suppressor • PLC1 overexpression
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