The study intends to investigate the regulation of syndecan-1 in human uterine leiomyoma cells. Human syndecan-1 levels were detected by Western blot in uterus leimyoma's tissue. The efficacy of syndecan-1 silencing on the cell proliferation, metalloproteinases and extracellular matrix were determined through Cell Counting Kit (CCK8) assay and Western blot assay, respectively. We compared the respective and combined effect of mifepristone and syndecan-1 on cell proliferation and the expression of metalloproteinases and extracellular matrix (ECM) in human uterine leiomyoma cells. The inhibitory effects of Syndecan-1 silencing on proliferation, ECM and Matrix Metalloproteinase (MMP) were observed in human uterine leiomyoma cells. Furthermore, syndecan-1 inhibition enhanced the effects of mifepristone against uterine leiomyoma cell proliferation. The expression of MMPs and ECM components in human uterine leiomyoma cells was decreased dramatically after syndecan-1 silencing, which was promoted after mifepristone treatment. Altogether, syndecan-1 silencing enhanced the efficacy of mifepristone on the uterine leiomyoma cell proliferation and ECM formation. Therefore, targeting syndecan-1 represents a novel therapeutic strategy to treat uterine leiomyoma.

该研究旨在研究 syndecan-1 在人子宫平滑肌瘤细胞中的调节作用。通过蛋白质印迹法检测子宫平滑肌瘤组织中的人 syndecan-1 水平。分别通过细胞计数试剂盒 (CCK8) 测定和蛋白质印迹测定确定 syndecan-1 沉默对细胞增殖、金属蛋白酶和细胞外基质的功效。我们比较了米非司酮和 syndecan-1 对人子宫平滑肌瘤细胞中细胞增殖以及金属蛋白酶和细胞外基质 (ECM) 表达的各自和联合作用。在人子宫平滑肌瘤细胞中观察到 Syndecan-1 沉默对增殖、ECM 和基质金属蛋白酶 (MMP) 的抑制作用。此外，syndecan-1 抑制增强了米非司酮对子宫平滑肌瘤细胞增殖的作用。syndecan-1 沉默后，人子宫平滑肌瘤细胞中 MMP 和 ECM 成分的表达显着降低，米非司酮治疗促进了这种表达。总之，syndecan-1 沉默增强了米非司酮对子宫平滑肌瘤细胞增殖和 ECM 形成的功效。因此，靶向 syndecan-1 代表了一种治疗子宫平滑肌瘤的新治疗策略。