Role of B-Cell Translocation Gene 1 in the Pathogenesis of Endometriosis

• Main Authors: Jeong Sook Kim, Young Sik Choi, Ji Hyun Park, Jisun Yun, Soohyun Kim, Jae Hoon Lee, Bo Hyon Yun, Joo Hyun Park, Seok Kyo Seo, SiHyun Cho, Hyun-Soo Kim, Byung Seok Lee
• Format: Article
• Language: English
• Published: MDPI AG 2019-07-01
• Series: International Journal of Molecular Sciences
• Subjects: BTG1; endometriosis; human endometrial stromal cells
• Online Access: https://www.mdpi.com/1422-0067/20/13/3372

Estrogen affects endometrial cellular proliferation by regulating the expression of the <i>c-myc</i> gene. B-cell translocation gene 1 (BTG1), a translocation partner of the <i>c-myc</i>, is a tumor suppressor gene that promotes apoptosis and negatively regulates cellular proliferation and cell-to-cell adhesion. The aim of this study was to determine the role of BTG1 in the pathogenesis of endometriosis. <i>BTG1</i> mRNA and protein expression was evaluated in eutopic and ectopic endometrium of 30 patients with endometriosis (endometriosis group), and in eutopic endometrium of 22 patients without endometriosis (control group). The effect of BTG1 downregulation on cellular migration, proliferation, and apoptosis was evaluated using transfection of primarily cultured human endometrial stromal cells (HESCs) with <i>BTG1</i> siRNA. <i>BTG1</i> mRNA expression level of eutopic and ectopic endometrium of endometriosis group were significantly lower than that of the eutopic endometrium of the control group. Migration and wound healing assays revealed that BTG1 downregulation resulted in a significant increase in migration potential of HESCs, characterized by increased expression of matrix metalloproteinase 2 (MMP2) and MMP9. Downregulation of BTG1 in HESCs significantly reduced Caspase 3 expression, indicating a decrease in apoptotic potential. In conclusion, our data suggest that downregulation of BTG1 plays an important role in the pathogenesis of endometriosis.