关键词: GATA2 endometrial cancer melatonin metastasis tumor proliferation

Mesh : Humans Female Melatonin / pharmacology GATA2 Transcription Factor / genetics metabolism Endometrial Neoplasms / drug therapy genetics metabolism Cell Proliferation Cell Line, Tumor

来  源:   DOI:10.1111/jpi.12918

Abstract:
Endometrial cancer (EC) is a reproductive system disease that occurs in perimenopausal and postmenopausal women. However, its etiology is unclear. Melatonin (MT) has been identified as a therapeutic agent for EC; however, its exact mechanism remains unclear. In the present study, we determined that GATA-binding protein 2 (GATA2) is expressed at low levels in EC and regulated by MT. MT upregulates the expression of GATA2 through MT receptor 1A (MTNR1A), whereas GATA2 can promote the expression of MTNR1A by binding to its promoter region. In addition, in vivo and in vitro experiments showed that MT inhibited the proliferation and metastasis of EC cells by upregulating GATA2 expression. The protein kinase B (AKT) pathway was also affected. In conclusion, these findings suggest that MT and GATA2 play significant roles in EC development.
摘要:
子宫内膜癌(EC)是一种发生在围绝经期和绝经后妇女的生殖系统疾病。然而,其病因尚不清楚。褪黑激素(MT)已被确定为EC的治疗剂;然而,其确切机制尚不清楚。在本研究中,我们确定GATA结合蛋白2(GATA2)在EC中低水平表达并受MT调节。MT通过MT受体1A(MTNR1A)上调GATA2的表达,而GATA2可以通过与其启动子区结合来促进MTNR1A的表达。此外,体内和体外实验表明,MT通过上调GATA2表达抑制EC细胞的增殖和转移。蛋白激酶B(AKT)通路也受到影响。总之,这些发现表明MT和GATA2在EC发展中起重要作用。
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