Downregulation of SPOCK2 promotes the proliferation, adhesion, and invasion of endometrial epithelial cells

A previous study found that a lack of SPOCK2 expression was an early event that occurs during the malignant transformation of endometriosis (EMS); however, the role played by SPOCK2 in the pathogenesis of endometriosis and its malignant transformation remains unclear. In this study, SPOCK2 expression in human endometrial epithelial cells (hEECs) was downregulated by transfection with shRNA, and the biological behavior of the transfected cells was observed. We found that downregulation of SPOCK2 promoted cell proliferation, adhesion, and invasion. Our data suggest that downregulation of SPOCK2 might participate in the pathogenesis and progression of EMS, as well as its malignant transformation, by promoting the proliferation, adhesion, and invasion of endometrial epithelial cells.

既往研究发现，SPOCK2表达缺失是子宫内膜异位症（Endometriosis, EMS）发生恶性转化过程中的早期事件；然而，SPOCK2在子宫内膜异位症及其恶性转化的发病机制中所发挥的作用仍不明确。本研究通过短发夹RNA（short hairpin RNA, shRNA）转染技术下调人子宫内膜上皮细胞（human endometrial epithelial cells, hEECs）中的SPOCK2表达，并观察转染后细胞的生物学行为。研究结果显示，SPOCK2表达下调可促进细胞增殖、黏附与侵袭。本研究数据提示，SPOCK2表达下调可能通过促进子宫内膜上皮细胞的增殖、黏附与侵袭，参与子宫内膜异位症的发病、进展及其恶性转化过程。