2021
DOI: 10.1016/j.canlet.2021.01.013
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Targeting FAPα-expressing tumor-associated mesenchymal stromal cells inhibits triple-negative breast cancer pulmonary metastasis

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Cited by 17 publications
(15 citation statements)
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“…Triple negative breast cancer (TNBC) is the most malignant subtype of breast cancer that seriously threatens women’s health and lives, and its associated morbidity and mortality have been increasing in recent years [ 1 , 2 ]. Metastasis is one of the main causes of failure in the treatment of TNBC [ 3 , 4 ]. Substantial studies evidenced that platelets support tumor metastatic progression by inducing epithelial-mesenchymal transition (EMT) of cancer cells and by shielding circulating tumor cells from immune-mediated elimination [ 5 , 6 ].…”
Section: Introductionmentioning
confidence: 99%
“…Triple negative breast cancer (TNBC) is the most malignant subtype of breast cancer that seriously threatens women’s health and lives, and its associated morbidity and mortality have been increasing in recent years [ 1 , 2 ]. Metastasis is one of the main causes of failure in the treatment of TNBC [ 3 , 4 ]. Substantial studies evidenced that platelets support tumor metastatic progression by inducing epithelial-mesenchymal transition (EMT) of cancer cells and by shielding circulating tumor cells from immune-mediated elimination [ 5 , 6 ].…”
Section: Introductionmentioning
confidence: 99%
“…Direct cellular interaction between mesenchymal stem cells (MSCs) and triple-negative breast cancer (TNBC) cells have been shown to trigger the epithelial-mesenchymal transition (EMT) process in TNBC cells. This transition enhances their invasive and metastatic properties [ 12 , 13 , 14 ]. In addition, MSCs can transmit mitochondria to TNBC cells using either tunneling nanotubes or extracellular vesicles.…”
Section: Effect Of Mscs On Tnbc Cells and Their Tumor Microenvironmen...mentioning
confidence: 99%
“…Therefore, comprehending the mechanisms and ramifications underlying the interplay between MSCs and TNBC assumes paramount importance in devising innovative therapeutic modalities for TNBC [ 13 , 18 ]. By targeting pivotal molecules implicated in this interplay (including, but not limited to, interleukin-6 (IL-6), prostaglandin E2 (PGE2), transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), and fibroblast activation protein alpha (FAPα) [ 13 ]), novel prospects for surmounting the challenges posed by this formidable breast cancer subtype may emerge.…”
Section: Effect Of Mscs On Tnbc Cells and Their Tumor Microenvironmen...mentioning
confidence: 99%
“…Different sources of CaMSCs all showed immunosuppressive effects, and the targets include macrophages, T-cells, and natural killer (NK) cells. Breast CaMSCs highly expressed FAPα and increased pulmonary metastasis by recruitment of M2 tumor-associated macrophages (TAM), which were identified by F4/80 and CCR2-positive population [ 58 ]. GC-MSC-primed M2 macrophages promoted the migration, invasion, and EMT of gastric cancer cells through secretion of IL-6 and IL-8, and the JAK2/STAT3 signaling pathway [ 59 ].…”
Section: T He Interaction Between Cancer-associated Mesench...mentioning
confidence: 99%