Exploring the interplay between triple-negative breast cancer stem cells and tumor microenvironment for effective therapeutic strategies

作者全名："Zou, Zhuoling; Luo, Tinglan; Wang, Xinyuan; Wang, Bin; Li, Qing"

作者地址："[Zou, Zhuoling] Nanchang Univ, Queen Mary Coll, Nanchang, Jiangxi, Peoples R China; [Luo, Tinglan; Wang, Bin] Chongqing Univ Technol, Affiliated Cent Hosp, Peoples Hosp Chongqing 7, Dept Oncol, 1 Mawangping St, Chongqing 401320, Peoples R China; [Wang, Xinyuan] Chongqing Med Univ, Dept Clin Med, Clin Coll 2, Chongqing, Peoples R China; [Li, Qing] Nanchang Univ, Affiliated Hosp 2, Dept Oncol, 1 Minde Rd, Nanchang 330000, Jiangxi, Peoples R China"

通信作者："Wang, B (通讯作者)，Chongqing Univ Technol, Affiliated Cent Hosp, Peoples Hosp Chongqing 7, Dept Oncol, 1 Mawangping St, Chongqing 401320, Peoples R China.; Li, Q (通讯作者)，Nanchang Univ, Affiliated Hosp 2, Dept Oncol, 1 Minde Rd, Nanchang 330000, Jiangxi, Peoples R China."

来源：JOURNAL OF CELLULAR PHYSIOLOGY

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:001233475100001

JCR分区：Q1

影响因子：5.6

年份：2024

卷号：239

期号：8

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结束页：　

文献类型：Review

关键词：cancer stem cells; drug resistance; treatment; triple-negative breast cancer; tumor microenvironment

摘要："Triple-negative breast cancer (TNBC) is a highly aggressive and metastatic malignancy with poor treatment outcomes. The interaction between the tumor microenvironment (TME) and breast cancer stem cells (BCSCs) plays an important role in the development of TNBC. Owing to their ability of self-renewal and multidirectional differentiation, BCSCs maintain tumor growth, drive metastatic colonization, and facilitate the development of drug resistance. TME is the main factor regulating the phenotype and metastasis of BCSCs. Immune cells, cancer-related fibroblasts (CAFs), cytokines, mesenchymal cells, endothelial cells, and extracellular matrix within the TME form a complex communication network, exert highly selective pressure on the tumor, and provide a conducive environment for the formation of BCSC niches. Tumor growth and metastasis can be controlled by targeting the TME to eliminate BCSC niches or targeting BCSCs to modify the TME. These approaches may improve the treatment outcomes and possess great application potential in clinical settings. In this review, we summarized the relationship between BCSCs and the progression and drug resistance of TNBC, especially focusing on the interaction between BCSCs and TME. In addition, we discussed therapeutic strategies that target the TME to inhibit or eliminate BCSCs, providing valuable insights into the clinical treatment of TNBC."

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