文章：

P53突变诱导输卵管细胞发生上皮-间质转化（EMT），该转化与干细胞特性及肿瘤发生相关

P53 Mutation Induces Epithelial-to-Mesenchymal Transition (EMT) Associated with Stem Cell Properties and Tumorigenesis in Fallopian Tube Cells

原文发布日期：14 October 2025

DOI: 10.3390/cancers17203317

类型: Article

开放获取: 是

英文摘要：

Background/Objectives: Type II ovarian cancer, including high-grade serous carcinoma (HGSC), is genetically unstable and exhibits frequent mutations in the tumor suppressor genes. Mutations ofTP53andBRCA1genes have been associated with HGSC, which has been suggested as a subtype that arises from the fallopian tube lesion called serous tubal intraepithelial carcinoma (STIC). AlthoughTP53andBRCA1genes are well-known tumor suppressor genes, the actual effects ofTP53andBRCA1mutations in enhancing the development of ovarian cancer initiated from STIC are poorly understood.Methods:In this study, we knocked outTrp53andBrca-1in epithelial cell clones derived from mice fallopian tube tissues (known as oviducts) and investigated the potential involvement of these two mutations in inducing cancer stem-like cells as cancer-initiating cells.Results:We have shown that the knockout ofTrp53induced oviduct cells to undergo EMT and acquire stem cell characteristics.Conclusions:Trp53mutation may induce the early stage of precursor lesions formation at the distal end of the oviducts.

摘要翻译： 

背景/目的：II型卵巢癌，包括高级别浆液性癌（HGSC），具有遗传不稳定性，并在肿瘤抑制基因中表现出频繁的突变。TP53和BRCA1基因的突变与HGSC相关，该亚型被认为起源于输卵管病变，称为浆液性输卵管上皮内癌（STIC）。尽管TP53和BRCA1基因是众所周知的肿瘤抑制基因，但TP53和BRCA1突变在促进由STIC引发的卵巢癌发展中的实际作用尚不清楚。方法：在本研究中，我们敲除了源自小鼠输卵管组织（称为输卵管）的上皮细胞克隆中的Trp53和Brca-1，并研究了这两种突变在诱导癌症干细胞作为癌症起始细胞中的潜在作用。结果：我们已经证明，敲除Trp53可诱导输卵管细胞发生上皮间质转化并获得干细胞特性。结论：Trp53突变可能诱导输卵管远端前体病变形成的早期阶段。

原文链接：

P53 Mutation Induces Epithelial-to-Mesenchymal Transition (EMT) Associated with Stem Cell Properties and Tumorigenesis in Fallopian Tube Cells