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利用生物信息学分析探讨威尔姆斯瘤（WT1）（+/KTS）变体促进卵巢上皮细胞增殖和迁移的分子机制。

Molecular mechanism of Wilms' tumor (Wt1) (+/-KTS) variants promoting proliferation and migration of ovarian epithelial cells by bioinformatics analysis.

机构信息

College of Basic Medicine, Jining Medical University, Jining, China.

Collaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, China.

出版信息

J Ovarian Res. 2023 Feb 24;16(1):46. doi: 10.1186/s13048-023-01124-2.

DOI:10.1186/s13048-023-01124-2
PMID:36829196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9951437/
Abstract

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.

摘要

上皮性卵巢癌 (EOC) 是一种死亡率最高的妇科疾病。由于对其发病机制缺乏了解，目前尚未建立针对 EOC 的准确早期诊断和筛查方法。研究揭示了 Wilms' 肿瘤 (Wt1) 基因在癌症中的多方面功能，这可能与存在多种选择性剪接有关。我们的研究结果表明，Wt1 (+KTS) 或 Wt1 (-KTS) 的过表达可显著促进人卵巢上皮细胞 HOSEpiC 的增殖和迁移，而 Wt1 (+KTS) 的作用更为明显。为了探讨 Wt1 (+/-KTS) 变异在上皮性卵巢癌 (OC) 发生和发展中的作用机制，本研究通过转录组测序探讨了 Wt1 (+/-KTS) 在上皮性卵巢癌细胞增殖和迁移中的差异调控。通过生物信息学分析筛选 OC 相关的枢纽基因，进一步探讨 Wt1 (+/-KTS) 在 OC 发生中的差异分子机制。最后，我们发现 Wt1 (+/-KTS) 变异对上皮性卵巢癌细胞增殖和迁移的调节可能通过不同的基因和信号通路发挥作用，并筛选出调节卵巢上皮细胞恶性转化的关键基因和差异调控基因。本研究的实施将为 OC 的早期诊断和精确治疗提供新的线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/aabf3d384b45/13048_2023_1124_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/7af2a7c8ba46/13048_2023_1124_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/911cd8337ef9/13048_2023_1124_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/dda3cc750934/13048_2023_1124_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/79f3c3768cd3/13048_2023_1124_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/57bb0cfe32f7/13048_2023_1124_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/aabf3d384b45/13048_2023_1124_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/7af2a7c8ba46/13048_2023_1124_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/c6ae5c1dba86/13048_2023_1124_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/7d77aca0c55d/13048_2023_1124_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/911cd8337ef9/13048_2023_1124_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/dda3cc750934/13048_2023_1124_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/79f3c3768cd3/13048_2023_1124_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/57bb0cfe32f7/13048_2023_1124_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9951437/aabf3d384b45/13048_2023_1124_Fig8_HTML.jpg

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