Innate Immune Program in Formation of Tumor-Initiating Cells from Cells-of-Origin of Breast, Prostate, and Ovarian Cancers.
Innate Immune Program in Formation of Tumor-Initiating Cells from Cells-of-Origin of Breast, Prostate, and Ovarian Cancers.
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DOI：
10.3390/cancers15030757
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发表时间：
2023-01-26
期刊：
影响因子：
5.2
通讯作者：
Li, Zhe
中科院分区：
文献类型：
--
作者：
Han, Sen;Chen, Xueqing;Li, Zhe
关键词：
肿瘤起始细胞，也称为癌症干细胞，是肿瘤中维持肿瘤的癌细胞的子集，并且通常负责治疗抗性和复发。在发育上，它们是从其相应癌症类型的细胞起源进化而来的，因此，可能从细胞起源继承一些表达程序。这篇综述旨在总结文献中的数据，这些数据表明几种与乳腺癌相关的癌症（即，乳腺、前列腺和卵巢）具有优选的腔祖细胞来源。这些管腔祖细胞表达共同的先天免疫程序（例如，Toll样受体及其相关基因）。源自此类管腔祖细胞的肿瘤起始细胞可以继承该程序，这可以通过Toll样受体途径的激活和与免疫细胞的串扰（例如，巨噬细胞）。我们提出了一种潜在的策略，通过进一步激活其遗传的先天免疫途径来增强免疫治疗，从而消除这种肿瘤起始细胞。肿瘤起始细胞（TICs），也称为癌症干细胞（CSCs），是可以引发肿瘤、具有自我更新能力并且可以促成肿瘤异质性的癌细胞。TIC/CSC是从它们的起源细胞发育而来的。在乳腺癌、前列腺癌和卵巢癌中，乳腺肺泡细胞、前列腺腔（分泌）细胞和输卵管分泌细胞的祖细胞是其相应癌症类型的优选细胞来源。这些管腔祖细胞（LP）表达共同的先天免疫程序（例如，Toll样受体（TLR）信号传导）相关基因。现在在乳腺、前列腺和输卵管组织及其相应的癌症类型中发现了细菌等微生物，这增加了它们的脂蛋白可能感知到微生物的存在并触发它们的先天免疫/TLR途径，导致炎症微环境的可能性。免疫细胞之间的串扰（例如，巨噬细胞）和受影响的上皮细胞（例如，LPs）最终可能部分通过STAT 3和/或NFκB途径促进由其相应的LPs形成TIC/CSC。因此，TIC/CSC可以从它们的起源细胞继承先天免疫/TLR途径相关基因的表达;先天免疫程序也可以代表它们独特的脆弱性，这可以在治疗上进行探索（例如，通过增强TLR信号传导增强免疫疗法）。
Tumor-initiating cells, also known as cancer stem cells, are a subset of cancer cells in a tumor that sustain the tumor and are often responsible for therapy resistance and relapse. Developmentally, they are evolved from the cellular origin of their corresponding cancer type and, as a result, may inherit some expression programs from the cellular origin. This review aims to summarize data from the literature showing that several hormone-related cancers (i.e., breast, prostate, and ovarian) have a preferred luminal progenitor origin. These luminal progenitors express a common innate immune program (e.g., Toll-like receptors and their associated genes). Tumor-initiating cells originated from such luminal progenitors may inherit this program, which may contribute to their formation via activation of Toll-like receptor pathways and crosstalk with immune cells (e.g., macrophages). We propose a potential strategy to eliminate such tumor-initiating cells by enhancing immunotherapy via further activation of their inherited innate immune pathways. Tumor-initiating cells (TICs), also known as cancer stem cells (CSCs), are cancer cells that can initiate a tumor, possess self-renewal capacity, and can contribute to tumor heterogeneity. TICs/CSCs are developed from their cells-of-origin. In breast, prostate, and ovarian cancers, progenitor cells for mammary alveolar cells, prostate luminal (secretory) cells, and fallopian tube secretory cells are the preferred cellular origins for their corresponding cancer types. These luminal progenitors (LPs) express common innate immune program (e.g., Toll-like receptor (TLR) signaling)-related genes. Microbes such as bacteria are now found in breast, prostate, and fallopian tube tissues and their corresponding cancer types, raising the possibility that their LPs may sense the presence of microbes and trigger their innate immune/TLR pathways, leading to an inflammatory microenvironment. Crosstalk between immune cells (e.g., macrophages) and affected epithelial cells (e.g., LPs) may eventually contribute to formation of TICs/CSCs from their corresponding LPs, in part via STAT3 and/or NFκB pathways. As such, TICs/CSCs can inherit expression of innate-immunity/TLR-pathway-related genes from their cells-of-origin; the innate immune program may also represent their unique vulnerability, which can be explored therapeutically (e.g., by enhancing immunotherapy via augmenting TLR signaling).
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影响因子：
--
作者：
Shuang C;Weiguang Y;Zhenkun F;Yike H;Jiankun Y;Jing X;Xinghan L;Yue L;Dalin L
通讯作者：
Dalin L
DOI：
10.1038/nrc4019
发表时间：
2015-11
期刊：
Nature reviews. Cancer
影响因子：
--
作者：
Bowtell DD;Böhm S;Ahmed AA;Aspuria PJ;Bast RC Jr;Beral V;Berek JS;Birrer MJ;Blagden S;Bookman MA;Brenton JD;Chiappinelli KB;Martins FC;Coukos G;Drapkin R;Edmondson R;Fotopoulou C;Gabra H;Galon J;Gourley C;Heong V;Huntsman DG;Iwanicki M;Karlan BY;Kaye A;Lengyel E;Levine DA;Lu KH;McNeish IA;Menon U;Narod SA;Nelson BH;Nephew KP;Pharoah P;Powell DJ Jr;Ramos P;Romero IL;Scott CL;Sood AK;Stronach EA;Balkwill FR
通讯作者：
Balkwill FR
DOI：
10.1186/bcr3593
发表时间：
2014-01-07
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Chang TH;Kunasegaran K;Tarulli GA;De Silva D;Voorhoeve PM;Pietersen AM
通讯作者：
Pietersen AM
DOI：
10.1084/jem.20031076
发表时间：
2003-10-06
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Akashi S;Saitoh S;Wakabayashi Y;Kikuchi T;Takamura N;Nagai Y;Kusumoto Y;Fukase K;Kusumoto S;Adachi Y;Kosugi A;Miyake K
通讯作者：
Miyake K
影响因子：
11.2
作者：
Collins, AT;Berry, PA;Maitland, NJ
通讯作者：
Maitland, NJ