Melatonin suppresses tumor proliferation and metastasis by targeting GATA2 in endometrial cancer

被引：5

作者：

Liao, Yangyou ^{[1
]}

Li, Ruiling ^{[1
]}

Pei, Jingyuan ^{[1
]}

Zhang, Juan ^{[1
]}

Chen, Bo ^{[1
]}

Dong, Haojie ^{[1
]}

Feng, Xiaoyu ^{[1
]}

Zhang, Hongshuo ^{[1
]}

Shang, Yuhong ^{[2
]}

Sui, Linlin ^{[1
]}

Kong, Ying ^{[1
]}

机构：

[1] Dalian Med Univ, Coll Basic Med Sci, Core Lab Glycobiol & Glycoengineering, Dalian, Peoples R China

[2] Dalian Med Univ, Affiliated Hosp 1, Dept Gynecol, Dalian, Liaoning, Peoples R China

来源：

JOURNAL OF PINEAL RESEARCH | 2024年 / 76卷 / 01期

关键词：

endometrial cancer; GATA2; melatonin; metastasis; tumor proliferation; RECEPTOR; BREAST; EXPRESSION; MT1; AGGRESSIVENESS; PREVENTION; ESTROGEN; GROWTH;

D O I：

10.1111/jpi.12918

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页数：15

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