表皮卵巢癌（EOC）是一种致命的妇科疾病。由于对其发病机制缺乏理解，因此目前没有确切的早期诊断和筛查方法。研究揭示了威尔姆斯肿瘤（Wt1）基因在癌症中的多方面功能，可能与多个选择性剪接体的存在有关。我们的研究结果表明，Wt1（+KTS）或Wt1（-KTS）的过度表达可以显著促进人卵巢上皮细胞HOSEpiC的增殖和迁移，而Wt1（+KTS）的效应更为明显。为了探索Wt1（+/-KTS）变异体在HOSEpiC增殖和迁移以及卵巢癌（OC）发生和发展中的机制，本研究通过转录组测序探索了Wt1（+/-KTS）在HOSEpiC增殖和迁移中的差异调控。通过生物信息学分析筛选OC相关的中心基因，进一步探索Wt1（+/-KTS）在OC发生中的差异分子机制。最后，我们发现Wt1（+/-KTS）变异体对HOSEpiC的增殖和迁移的调控可能通过不同的基因和信号通路发挥作用，并筛选出关键基因和不同调控基因，这些基因调控了卵巢上皮细胞的恶性转化。本研究的实施将为OC的早期诊断和精准治疗提供新线索。© 2023. 作者（们）。

Epithelial ovarian cancer (EOC) is a gynecological disease with the highest mortality. With the lack of understanding of its pathogenesis, no accurate early diagnosis and screening method has been established for EOC. Studies revealed the multi-faceted function of Wilms' tumor (Wt1) genes in cancer, which may be related to the existence of multiple alternative splices. Our results show that Wt1 (+KTS) or Wt1 (-KTS) overexpression can significantly promote the proliferation and migration of human ovarian epithelial cells HOSEpiC, and Wt1 (+KTS) effects were more evident. To explore the Wt1 (+/-KTS) variant mechanism in HOSEpiC proliferation and migration and ovarian cancer (OC) occurrence and development, this study explored the differential regulation of Wt1 (+/-KTS) in HOSEpiC proliferation and migration by transcriptome sequencing. OC-related hub genes were screened by bioinformatics analysis to further explore the differential molecular mechanism of Wt1 (+/-KTS) in the occurrence of OC. Finally, we found that the regulation of Wt1 (+/-KTS) variants on the proliferation and migration of HOSEpiC may act through different genes and signaling pathways and screened out key genes and differentially regulated genes that regulate the malignant transformation of ovarian epithelial cells. The implementation of this study will provide new clues for the early diagnosis and precise treatment of OC.© 2023. The Author(s).