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논문 기본 정보

자료유형
학술저널
저자정보
Min-Ah Park (Chungbuk National University) Kyung-A Hwang (Chungbuk National University) Hye-Rim Lee (Chungbuk National University) Bo-Rim Yi (Chungbuk National University) Kyung-Chul Choi (Chungbuk National University)
저널정보
한국독성학회 Toxicological Research Toxicological Research Vol.27 No.4
발행연도
2011.12
수록면
253 - 259 (7page)

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초록· 키워드

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Transforming growth factor β?(TGF-β) is involved in cellular processes including growth, differentiation, apoptosis, migration, and homeostasis. Generally, TGF-β?is the inhibitor of cell cycle progression and plays a role in enhancing the antagonistic effects of many growth factors. Unlike the antiproliferative effect of TGF-β, E2, an endogeneous estrogen, is stimulating cell proliferation in the estrogen-dependent organs, which are mediated via the estrogen receptors, ERα?and ERβ, and may be considered as a critical risk factor in tumorigenesis of hormone-responsive cancers. Previous researches reported the cross-talk between estrogen/ERα?and TGF-β?pathway. Especially, based on the E2-mediated inhibition of TGF-β?signaling, we examined the inhibition effect of 4-tert-octylphenol (OP) and 4-nonylphenol (NP), which are well known xenoestrogens in endocrine disrupting chemicals (EDCs), on TGF-β?signaling via semi-quantitative reverse-transcription PCR. The treatment of E2, OP, or NP resulted in the downregulation of TGF-β?receptor2 (TGF-β?R2) in TGF-β?signaling pathway. However, the expression level of TGF-β1 and TGF-β?receptor1 (TGF-β?R1) genes was not altered. On the other hand, E2, OP, or NP upregulated the expression of a cell-cycle regulating gene, c-myc, which is a oncogene and a downstream target gene of TGF-β?signaling pathway. As a result of downregulation of TGF-β?R2 and the upregulation of c-myc, E2, OP, or NP increased cell proliferation of BG-1 ovarian cancer cells. Taken together, these results suggest that E2 and these two EDCs may mediate cancer cell proliferation by inhibiting TGF-β?signaling via the downregulation of TGF-β?R2 and the upregulation of c-myc oncogene. In addition, it can be inferred that these EDCs have the possibility of tumorigenesis in estrogen-responsive organs by certainly representing estrogenic effect in inhibiting TGF-β?signaling.

목차

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES

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