The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.

中文翻译：

---

ARHGAP30 的敲低通过抑制 PI3K/AKT/mTOR 信号通路来抑制卵巢癌细胞的增殖、迁移和侵袭。

卵巢癌 (OC) 的死亡率和发病率很高，但 OC 的潜在机制尚未明确。在这项研究中，我们确定了 Rho GTP 酶激活蛋白 30 (ARHGAP30) 在 OC 进展中的作用。我们使用免疫组织化学 (IHC) 和 RT-qPCR 测量了 OC 组织样本和细胞中的 ARHGAP30 丰度。EdU、transwell 和膜联蛋白 V/PI 凋亡测定分别用于评估 OC 细胞的增殖、侵袭性和凋亡。结果表明，ARHGAP30 在 OC 组织样本和细胞中过表达。抑制 ARHGAP30 可抑制 OC 细胞的生长和转移，并增强细胞凋亡。OC 细胞中 ARHGAP30 的敲低显着抑制了 PI3K/AKT/mTOR 通路。用 PI3K/AKT/mTOR 通路抑制剂 buparlisib 处理可模拟 ARHGAP30 敲低对 OC 细胞生长、侵袭和凋亡的影响。buparlisib 治疗后，p-PI3K、p-AKT 和 p-mTOR 的表达水平显着降低。此外，buparlisib 抑制 ARHGAP30 上调对 OC 细胞生长和侵袭的影响。总之，ARHGAP30 调节 PI3K/AKT/mTOR 通路以促进 OC 的进展。