Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A

Galindo-Hernández, Octavio; Gonzales-Vazquez, Cristina; Cortés‐Reynosa, Pedro; Reyes-Uribe, Emmanuel; Chávez-Ocaña, Sonia; Reyes-Hernández, Octavio Daniel; Sierra-Martínez, Mónica; Salazar, Eduardo Pérez

doi:10.1007/s13277-015-3711-9

Cited by 15 publications

(14 citation statements)

References 40 publications

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“…Overexpression of N-cadherin in primary melanomas and the loss of E-cadherin expression in primary melanomas and metastatic melanomas correlated with worse overall survival of CM patients [18]. The absence of E-cadherin and the presence of N-cadherin in CM ectosomes may reflect their potential to induce or promote EMT in recipient cells and such properties have already been shown for exosomes released by bladder cancer cells [19] and exosomes from plasma of breast cancer patients [20]. Additionally, Qendro et al [4] demonstrated that the pattern of vimentin expression in exosomes can help predict tumor aggressiveness in different subtypes of melanoma.…”

Section: Proteins Involved In Cancer Progression Detected In Cm-derivmentioning

confidence: 67%

Mass Spectrometry-Based Proteomic Characterization of Cutaneous Melanoma Ectosomes Reveals the Presence of Cancer-Related Molecules

Surman

Kędracka–Krok

Hoja-Łukowicz

et al. 2020

IJMS

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Cutaneous melanoma (CM) is an aggressive type of skin cancer for which effective biomarkers are still needed. Recently, the protein content of extracellular vesicles (ectosomes and exosomes) became increasingly investigated in terms of its functional role in CM and as a source of novel biomarkers; however, the data concerning the proteome of CM-derived ectosomes is very limited. We used the shotgun nanoLC–MS/MS approach to the profile protein content of ectosomes from primary (WM115, WM793) and metastatic (WM266-4, WM1205Lu) CM cell lines. Additionally, the effect exerted by CM ectosomes on recipient cells was assessed in terms of cell proliferation (Alamar Blue assay) and migratory properties (wound healing assay). All cell lines secreted heterogeneous populations of ectosomes enriched in the common set of proteins. A total of 1507 unique proteins were identified, with many of them involved in cancer cell proliferation, migration, escape from apoptosis, epithelial–mesenchymal transition and angiogenesis. Isolated ectosomes increased proliferation and motility of recipient cells, likely due to the ectosomal transfer of different cancer-promoting molecules. Taken together, these results confirm the significant role of ectosomes in several biological processes leading to CM development and progression, and might be used as a starting point for further studies exploring their diagnostic and prognostic potential.

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Section: Proteins Involved In Cancer Progression Detected In Cm-derivmentioning

confidence: 67%

Mass Spectrometry-Based Proteomic Characterization of Cutaneous Melanoma Ectosomes Reveals the Presence of Cancer-Related Molecules

Surman

Kędracka–Krok

Hoja-Łukowicz

et al. 2020

IJMS

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“…O'Brien et al demonstrated that exosomes isolated from an invasive variant of triple negative breast cancer (TNBC) cells (Hs578Ts (i)8 ) caused an increase in the growth rate, migration, and invasive capacity of SKBR3, MDA-MB-231, and HCC1954 breast cancer cell lines, as well as causing an increase in endothelial cell angiogenesis [ 50 ]. Galindo-Hernandez et al reported that an epithelial-mesenchymal transition-like process was induced in MCF10A cells by EVs isolated from plasma of women with breast carcinoma [ 151 ]. Exosomes from the serum of patients with TNBC also produced significantly greater invasion of breast cancer cell lines compared to exosomes from healthy donors [ 50 ].…”

Section: Ev Contribution To Breast Tumor Growth and Metastasismentioning

confidence: 99%

Breast Cancer-Derived Extracellular Vesicles: Characterization and Contribution to the Metastatic Phenotype

Green

Alpaugh

Barsky

et al. 2015

BioMed Research International

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The study of extracellular vesicles (EVs) in cancer progression is a complex and rapidly evolving field. Whole categories of cellular interactions in cancer which were originally presumed to be due solely to soluble secreted molecules have now evolved to include membrane-enclosed extracellular vesicles (EVs), which include both exosomes and shed microvesicles (MVs), and can contain many of the same molecules as those secreted in soluble form but many different molecules as well. EVs released by cancer cells can transfer mRNA, miRNA, and proteins to different recipient cells within the tumor microenvironment, in both an autocrine and paracrine manner, causing a significant impact on signaling pathways, mRNA transcription, and protein expression. The transfer of EVs to target cells, in turn, supports cancer growth, immunosuppression, and metastasis formation. This review focuses exclusively on breast cancer EVs with an emphasis on breast cancer-derived exosomes, keeping in mind that breast cancer-derived EVs share some common physical properties with EVs of other cancers.

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“…As a result, intercellular contacts and apical-basal polarity are lost, and tumor cell motility is enhanced via reorganization of the actin cytoskeleton and the intermediate filament network (Thiery et al, 2009;May et al, 2011). EMT-associated transcription factors can also stimulate secretion of gelatinases and matrix metalloproteinases (MMPs), leading to remodeling of the extracellular matrix (ECM) (Galindo-Hernandez et al, 2015;Shen et al, 2017). The induction of EMT in carcinomas can further increase tumor angiogenesis via enriching CSCs which possess the capacity to differentiate into endothelial cells and also upregulate the expression of the pro-angiogenic transcription factor VEGF-A (Fantozzi et al, 2014;Delgado-Bellido et al, 2017).…”

Section: Escape From the Primary Tumor Site And Intravasation Into Thmentioning

confidence: 99%

Cellular Plasticity in Breast Cancer Progression and Therapy

Kong

Hughes

Ford

2020

Front. Mol. Biosci.

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With the exception of non-melanoma skin cancer, breast cancer is the most frequently diagnosed malignant disease among women, with the majority of mortality being attributable to metastatic disease. Thus, even with improved early screening and more targeted treatments which may enable better detection and control of early disease progression, metastatic disease remains a significant problem. While targeted therapies exist for breast cancer patients with particular subtypes of the disease (Her2+ and ER/PR+), even in these subtypes the therapies are often not efficacious once the patient's tumor metastasizes. Increases in stemness or epithelial-to-mesenchymal transition (EMT) in primary breast cancer cells lead to enhanced plasticity, enabling tumor progression, therapeutic resistance, and distant metastatic spread. Numerous signaling pathways, including MAPK, PI3K, STAT3, Wnt, Hedgehog, and Notch, amongst others, play a critical role in maintaining cell plasticity in breast cancer. Understanding the cellular and molecular mechanisms that regulate breast cancer cell plasticity is essential for understanding the biology of breast cancer progression and for developing novel and more effective therapeutic strategies for targeting metastatic disease. In this review we summarize relevant literature on mechanisms associated with breast cancer plasticity, tumor progression, and drug resistance.

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Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A

Cited by 15 publications

References 40 publications

Mass Spectrometry-Based Proteomic Characterization of Cutaneous Melanoma Ectosomes Reveals the Presence of Cancer-Related Molecules

Mass Spectrometry-Based Proteomic Characterization of Cutaneous Melanoma Ectosomes Reveals the Presence of Cancer-Related Molecules

Breast Cancer-Derived Extracellular Vesicles: Characterization and Contribution to the Metastatic Phenotype

Cellular Plasticity in Breast Cancer Progression and Therapy

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