Related Experiment Video
Updated: Jul 14, 2025

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Melatonin suppresses tumor proliferation and metastasis by targeting GATA2 in endometrial cancer
Yangyou Liao1, Ruiling Li1, Jingyuan Pei1
1Core Laboratory of Glycobiology and Glycoengineering, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
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.
Related Concept Videos
Abnormal Proliferation
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mitogens and the Cell Cycle
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

