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由不同的上皮-间质转化程序驱动的肿瘤异质性与协同癌症特征

Tumor Heterogeneity and Cooperating Cancer Hallmarks Driven by Divergent EMT Programs.

作者信息

Carter Phoebe, Kang Yibin

机构信息

Department of Molecular Biology, Princeton University, Princeton, New Jersey.

Ludwig Institute for Cancer Research Princeton Branch, Princeton, New Jersey.

出版信息

Cancer Res. 2025 Jan 2;85(1):12-14. doi: 10.1158/0008-5472.CAN-24-4309.

DOI:10.1158/0008-5472.CAN-24-4309
PMID:39546766
Abstract

Epithelial-to-mesenchymal transition (EMT) is known to play roles in orchestrating cellular plasticity across many physiological and pathological contexts. Partial EMT, wherein cells maintain both epithelial and mesenchymal features, is gaining recognition for its functional importance in cancer in recent years. There are many factors regulating both partial and full EMT, and the precise mechanisms underlying these processes vary depending on the biological context. Furthermore, how different EMT states cooperate to create a heterogeneous tumor population and promote different pro-malignant features remains largely undefined. In a recent study published in Nature Cancer, Youssef and colleagues described how two disparate EMT programs, active in either organ fibrosis or embryonic development, are utilized within different cells within the same murine mammary tumor model. This work provides mechanistic insight into the development of intratumoral heterogeneity, providing evidence for the cooperation between the two EMT trajectories.

摘要

上皮-间质转化(EMT)在许多生理和病理环境中协调细胞可塑性方面发挥作用。近年来,部分EMT(细胞同时保留上皮和间质特征)因其在癌症中的功能重要性而受到越来越多的关注。有许多因素调节部分和完全EMT,这些过程的精确机制因生物学背景而异。此外,不同的EMT状态如何协同作用以产生异质性肿瘤群体并促进不同的促癌特征,在很大程度上仍不明确。在最近发表于《自然·癌症》杂志的一项研究中,优素福及其同事描述了在同一小鼠乳腺肿瘤模型的不同细胞中,如何利用在器官纤维化或胚胎发育中活跃的两种不同的EMT程序。这项工作为肿瘤内异质性的发展提供了机制性见解,为两种EMT轨迹之间的合作提供了证据。

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