Ovarian cancer (OC) is a common gynecologic malignancy worldwide. Several members of the tripartite motif (TRIM) family are of great importance in various human malignancies. In this study, we aimed to figure out the function and mechanism of TRIM52 in OC. Western blot and RT–PCR were used to examine the expression level of TRIM52. Cell counting kit-8 (CCK-8) assay was used to measure cell proliferation. Annexin V/ PI kit and TUNEL assay were carried out to test cell apoptosis. Knockdown of TRIM52 significantly inhibited cell proliferation and induced cell apoptosis. Glucose uptake, lactate, and ATP production were depressed after TRIM52 silencing. Furthermore, loss of TRIM52 decreased the levels of pyruvate kinase isozyme M2, glucose transporter protein 1, and p-STAT3. Overexpression of TRIM52 showed effects that were opposite as those of TRIM52 knockdown; these effects were alleviated by AG490, which is an inhibitor of STAT3. In addition, TRIM52 knockdown inhibited tumorigenesis in a xenograft mouse model. Finally, we found that high level of TRIM52 expression predicted poor prognosis. In conclusion, TRIM52 knockdown inhibited cell proliferation and induced apoptosis through the activation of STAT3 signaling.

卵巢癌（OC）是世界范围内常见的妇科恶性肿瘤。三方基序 (TRIM) 家族的几个成员在各种人类恶性肿瘤中非常重要。在本研究中，我们旨在弄清楚TRIM52在OC中的功能和机制。使用蛋白质印迹和 RT-PCR 检测 TRIM52 的表达水平。细胞计数试剂盒-8 (CCK-8) 测定用于测量细胞增殖。进行Annexin V/PI试剂盒和TUNEL法检测细胞凋亡。TRIM52的敲低显着抑制细胞增殖并诱导细胞凋亡。TRIM52 沉默后，葡萄糖摄取、乳酸和 ATP 产生受到抑制。此外，TRIM52 的缺失降低了丙酮酸激酶同工酶 M2、葡萄糖转运蛋白 1 和 p-STAT3 的水平。TRIM52 的过表达显示出与 TRIM52 敲低相反的效果；AG490（一种 STAT3 抑制剂）可减轻这些影响。此外，TRIM52 敲低抑制了异种移植小鼠模型中的肿瘤发生。最后，我们发现高水平的 TRIM52 表达预示着预后不良。总之，TRIM52 敲低通过激活 STAT3 信号传导抑制细胞增殖并诱导细胞凋亡。