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TERT mRNA Expression is Up-Regulated in MCF-7 Cells and a Mouse Mammary Organ Culture (MMOC) System by Endosulfan Treatment
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  • TERT mRNA Expression is Up-Regulated in MCF-7 Cells and a Mouse Mammary Organ Culture (MMOC) System by Endosulfan Treatment
  • TERT mRNA Expression is Up-Regulated in MCF-7 Cells and a Mouse Mammary Organ Culture (MMOC) System by Endosulfan Treatment
저자명
Je. Kang Hoon,Kim. Ki Nam,Nam. Kung Woo,Cho. Myung Haing,Mar. Woong Chon
간행물명
Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea
권/호정보
2005년|28권 3호|pp.351-357 (7 pages)
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대한약학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Endosulfan is one of the organochlorine pesticides, which are well-known endocrine disruptors (EDs), and it acts as an estrogen agonist. Estrogen is a group of hormones that play an important role in mammary gland function and are implicated in mammary carcinogenesis. In the present study, we studied the effects of endosulfan on nodule like alveolar lesion (NLAL) formation in mouse mammary gland development using a mouse mammary gland organ culture (MMOC) system. Although endosulfan-treated mammary glands did not form NLALs, more alveolar buds were formed in this group than in the negative control (vehicle-treated) group. In addition, telomerase reverse transcriptase (TERT) mRNA expression levels were increased in endosulfan-treated mammary glands in a dose-dependent manner. Telomerase can be activated by estrogen, therefore, we examined the effects of endosulfan on telomerase activity, and found that the telomerase activity in estrogen receptor-positive MCF-7 cells was up-regulated by endosulfan treatment. Moreover, this activation was accompanied by the up­regulation of the TERT mRNA expression. Also, transient expression assays using CAT reporter plasm ids containing various fragments of the TERT promoter showed that this imperfect palindromic estrogen-responsive element is almost certainly responsible for the transcriptional activation by endosulfan. These results may help elucidate the endocrine disrupting mechanism of endosulfan.