We aimed to investigate the effect of propofol on the growth of human ovarian cancer cells ES2 and OVCAR-3 in vitro by regulating long non-coding RNA HOST2 (human ovarian cancer-specific transcript 2) and the inhibition of JAK2/STAT3 signaling pathway. In the present study, ES-2 and OVCAR-3 cells were firstly treated with different concentrations of propofol (0, 1, 5 and 10 μg/ml). The expression of HOST2 in ES-2 and OVCAR-3 cells were detected by quantitative reverse transcription-PCR (qRT-PCR). Then, the expression of HOST2 was changed by transfection of HOST2 overexpression plasmid into ES-2 and OVCAR-3 cells. Cell proliferation, migration, invasion and apoptosis were performed using CCK-8, wound-healing, Transwell assays and Flow Cytometry. Western blot analysis was performed to detect the expressions of apoptosis-associated proteins and JAK2/STAT3 pathway-related proteins. Results showed that cell viability and intracellular HOST2 expression in ES-2 and OVCAR-3 cells were decreased gradually with the increase of propofol concentration in a dose-dependent manner. Compared with the propofol group, overexpression of HOST2 significantly promoted the cell proliferation, migration, invasion and inhibited apoptosis, and ameliorated the inhibitory effect of propofol on the growth of tumor cells. Western blot analysis showed that compared with propofol group, the expression of Bcl-2 was significantly increased whereas Bax and the ratio of Cleaved caspase3/caspase3 were significantly decreased in pcDNA-HOST2 group. In addition, overexpression of HOST2 significantly enhanced the phosphorylation level of JAK2 and STAT3, and reduced the suppressive effect of propofol on JAK2/STAT3 signaling. Our results illustrated that propofol could significantly inhibit the proliferation, migration, invasion and induce apoptosis of ES-2 and OVCAR-3 cells by downregulating HOST2. The regulation mechanism may be achieved by inhibiting the activation of JAK2/STAT3 signaling pathway.

我们旨在通过调控长链非编码RNA HOST2（人卵巢癌特异性转录本2）和抑制JAK2/STAT3信号通路，研究异丙酚对体外人卵巢癌细胞ES2和OVCAR-3生长的影响。在本研究中，首先用不同浓度的丙泊酚（0、1、5 和 10 μg/ml）处理 ES-2 和 OVCAR-3 细胞。通过定量逆转录PCR（qRT-PCR）检测HOST2在ES-2和OVCAR-3细胞中的表达。然后，通过将HOST2过表达质粒转染到ES-2和OVCAR-3细胞中来改变HOST2的表达。使用 CCK-8、伤口愈合、Transwell 测定和流式细胞术进行细胞增殖、迁移、侵袭和凋亡。进行蛋白质印迹分析以检测凋亡相关蛋白和JAK2/STAT3通路相关蛋白的表达。结果表明，随着丙泊酚浓度的增加，ES-2和OVCAR-3细胞的细胞活力和细胞内HOST2表达呈剂量依赖性逐渐​​降低。与丙泊酚组相比，过表达HOST2显着促进细胞增殖、迁移、侵袭，抑制细胞凋亡，改善丙泊酚对肿瘤细胞生长的抑制作用。Western blot分析显示，与丙泊酚组相比，pcDNA-HOST2组Bcl-2表达明显升高，Bax和Cleaved caspase3/caspase3比值明显降低。此外，HOST2 的过表达显着提高了 JAK2 和 STAT3 的磷酸化水平，并降低了丙泊酚对 JAK2/STAT3 信号传导的抑制作用。我们的研究结果表明，丙泊酚可通过下调 HOST2 显着抑制 ES-2 和 OVCAR-3 细胞的增殖、迁移、侵袭和诱导凋亡。该调控机制可能通过抑制JAK2/STAT3信号通路的激活来实现。