信号转导子和转录激活子 3 (STAT3) 在调节癌细胞增殖、存活和转移中发挥着关键作用。我们的目的是确定 YHO-1701（一种口服 STAT3 抑制剂）对卵巢癌 (OC) 的影响。我们使用标准细胞增殖评估了 YHO-1701 对患者来源细胞 (PDC) 和 OC 细胞系细胞生长的影响化验。使用三维 (3D) 细胞活力测定评估源自 PDC 的球体模型。在口服 20 mg/kg YHO-1701 治疗的 SKOV3 异种移植小鼠中进行了抗肿瘤活性。通过蛋白质印迹分析 STAT3 信号传导的变化。通过对 RNA 进行测序并使用靶向 STAT3 (STAT3 siRNA) 的小干扰 RNA (STAT3 siRNA) 和 YHO-1701 分析 SKOV3 中的通路，研究了 STAT3 抑制的分子机制。YHO-1701 通过阻止 STAT3 二聚化和降低 OC 细胞系的生长来抑制 OC 细胞系的生长。其下游信号分子生存素的表达。从原发性和复发性 OC 患者中获得的 PDC 和球体的生长受到显着抑制。 YHO-1701 在 SKOV3 异种移植小鼠中观察到抗肿瘤作用。 YHO-1701 诱导 OC 细胞凋亡。此外，在用 YHO-1701 孵育的 SKOV3 细胞和用 STAT3 siRNA 孵育的 SKOV3 细胞中，p53 和/或 MAPK 信号通路上调。我们的结果表明，YHO-1701 抑制 OC 的 PDC 中的细胞生长，并伴有生存素抑制和与对照组相比，YHO-1701 治疗小鼠腹膜转移的数量。因此，YHO-1701 可能是治疗 OC 的有前途的候选药物。© 2025。亚洲妇科肿瘤学会、韩国妇科肿瘤学会和日本妇科肿瘤学会。

Signal transducer and activator of transcription 3 (STAT3) plays key roles in regulating cancer cell proliferation, survival, and metastasis. We aimed to determine the effects of YHO-1701, an oral STAT3 inhibitor, in ovarian cancer (OC).We evaluated the impact of YHO-1701 on cell growth in patient-derived cells (PDCs) and OC cell lines using standard cell proliferation assays. Spheroid models derived from PDCs were assessed using three-dimensional (3D) cell viability assays. Antitumor activity was performed in SKOV3 xenograft mice treated orally administrated YHO-1701 with 20 mg/kg. Changes in STAT3 signaling were analyzed by western blotting. The molecular mechanisms of STAT3 inhibition were investigated by sequencing RNA and analyzing pathways in the SKOV3 using a small interfering RNA targeting STAT3 (STAT3 siRNA) and YHO-1701.YHO-1701 inhibited the growth of OC cell lines by preventing STAT3 dimerization and decreasing the expression of its downstream signaling molecule, survivin. The growth of PDCs and spheroids obtained from patients with primary and recurrent OCs was significantly inhibited. Antitumor effect was observed in the SKOV3 xenograft mice with YHO-1701. YHO-1701 induced apoptosis in OC cells. Additionally, p53 and/or MAPK signaling pathways were upregulated in SKOV3 cells incubated with YHO-1701 and in those with STAT3 siRNA.Our results showed that YHO-1701 suppressed cell growth in PDCs of OC, accompanied by survivin inhibition, and a decrease in the number of peritoneal metastasis in the mice by YHO-1701, compared with those treated with control. Therefore, YHO-1701 could be a promising candidate agent for treating OC.© 2025. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology, and Japan Society of Gynecologic Oncology.