Extracellular vesicles from MDA-MB-231 breast cancer cells stimulated with linoleic acid promote an EMT-like process in MCF10A cells

Galindo-Hernández, Octavio; Serna-Márquez, Nathalia; Castillo-Sánchez, Rocío; Salazar, Eduardo Pérez

doi:10.1016/j.plefa.2014.09.002

Cited by 62 publications

(66 citation statements)

References 51 publications

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“…Although not functionally validated, there is an association between exosomes derived from mesenchymal cells and induction of EMT in epithelial cells (Tauro et al, 2013). Similarly, EVs isolated from the metastatic breast cancer cell line MDA-MB-231 stimulated with linoleic acid induce an EMT-like process in epithelial MCF10A cells (Galindo-Hernandez et al, 2014). Elucidating the role of EVs in the regulation of cell polarity and the initiation of EMT in vivo requires intensive future investigation (Lakkaraju and Rodriguez-Boulan, 2008).…”

Section: Role Of Evs In Promoting Survival and Growth Of The Primary mentioning

confidence: 99%

Extracellular Vesicles in Cancer: Cell-to-Cell Mediators of Metastasis

et al. 2016

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Summary Tumor-secreted extracellular vesicles (EVs) are critical mediators of intercellular communication between tumor cells and stromal cells in local and distant microenvironments. Accordingly, EVs play an essential role in both primary tumor growth and metastatic evolution. EVs orchestrate multiple systemic pathophysiological processes, such as coagulation, vascular leakiness, and reprogramming of stromal recipient cells to support pre-metastatic niche formation and subsequent metastasis. Clinically, EVs may be biomarkers and novel therapeutic targets for cancer progression, particularly for predicting and preventing future metastatic development.

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Section: Role Of Evs In Promoting Survival and Growth Of The Primary mentioning

confidence: 99%

Extracellular Vesicles in Cancer: Cell-to-Cell Mediators of Metastasis

et al. 2016

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“…For example, EVs from the metastatic BCa line MDA-MB-231 treated with linoleic acid can initiate an EMTlike phenotypic switch in recipient nontumorigenic MCF10A cells, which display increased expression of N-cadherin, Sip1, Snail1/2, Twist1/2, and Vimentin. 59 Urothelial cells treated with bladder cancer-derived EVs have increased expression of mesenchymal markers -SMA, S100A4, and Snail, with simultaneous downregulation of epithelial markers -catenin and E-cadherin. 60 In addition, EVs prepared from patient urine and bladder barbotage samples can also induce the expression of several mesenchymal markers in recipient urothelial cells.…”

Section: Contributes To Tumor Progressionmentioning

confidence: 99%

“…Epithelial‐to‐mesenchymal transition (EMT), a process that not only allows epithelial cells to lose cellular polarity and intercellular adherence but also to gain migratory and invasive properties to become MSCs, can be induced by EVs in the TME. For example, EVs from the metastatic BCa line MDA‐MB‐231 treated with linoleic acid can initiate an EMT‐like phenotypic switch in recipient nontumorigenic MCF10A cells, which display increased expression of N‐cadherin, Sip1, Snail1/2, Twist1/2, and Vimentin . Urothelial cells treated with bladder cancer‐derived EVs have increased expression of mesenchymal markers α‐SMA, S100A4, and Snail, with simultaneous downregulation of epithelial markers β‐catenin and E‐cadherin .…”

Section: Ev‐mediated Intercellular Communication In the Tme Contributmentioning

confidence: 99%

Extracellular vesicles in the tumor microenvironment: Therapeutic resistance, clinical biomarkers, and targeting strategies

Han

et al. 2017

Medicinal Research Reviews

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Numerous studies have proved that cell‐nonautonomous regulation of neoplastic cells is a distinctive and essential characteristic of tumorigenesis. Two way communications between the tumor and the stroma, or within the tumor significantly influence disease progression and modify treatment responses. In the tumor microenvironment (TME), malignant cells utilize paracrine signaling initiated by adjacent stromal cells to acquire resistance against multiple types of anticancer therapies, wherein extracellular vesicles (EVs) substantially promote such events. EVs are nanoscaled particles enclosed by phospholipid bilayers, and can mediate intercellular communications between cancerous cells and the adjacent microenvironment to accelerate pathological proceeding. Here we review the most recent studies of EV biology and focus on key cell lineages of the TME and their EV cargoes that are biologically active and responsible for cancer resistance, including proteins, RNAs, and other potentially essential components. Since EVs are emerging as novel but critical elements in establishing and maintaining hallmarks of human cancer, timely and insightful understanding of their molecular properties and functional mechanisms would pave the road for clinical diagnosis, prognosis, and effective targeting in the global landscape of precision medicine. Further, we address the potential of EVs as promising biomarkers in cancer clinics and summarize the technical improvements in EV preparation, analysis, and imaging. We highlight the practical issues that should be exercised with caution to guide the development of targeting agents and therapeutic methodologies to minimize cancer resistance driven by EVs, thereby allowing to effectively control the early steps of disease exacerbation.

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“…53 A further study evaluated the occurrence of EMT in a nontumorigenic breast epithelial cell line after treatment with EVs derived from a highly invasive breast cancer cell line and showed that MDA-MB-231 breast cancer cells treated with linoleic acid release EVs that could induce EMT in nontumorigenic human mammary epithelial cells (MCF-10A), confirmed by downregulation of E-cadherin expression and upregulation of mesenchymal markers such as SNAIL1, SNAIL2, TWIST1 and 2, SIP1, vimentin and N-cadherin. 54 The MCF-10A cells treated with EVs secreted MMP-2 and MMP-9, enzymes capable of degrading the extracellular matrix, an important event for the initiation of migration and invasion. 54 Although previous studies have shown that cancer-derived exosomes may contribute to the epithelial-mesenchymal transition (EMT) in untransformed cells, few studies have defined the exosome cargo upon EMT induction.…”

Section: Epithelial-mesenchymal Transition Induced By Cancer Cell Exomentioning

confidence: 99%

The multifaceted role of extracellular vesicles in metastasis: Priming the soil for seeding

et al. 2017

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Extracellular vesicles (EVs), including exosomes, play a key role in inter and intracellular communication, promoting the proliferation and invasion of recipient cells to support tumor growth and metastasis. Metastasis comprises multiple steps that first include the detachment of tumor cells through epithelial to mesenchymal transition (EMT), allowing the physical dissemination to distant organs. Thereafter, cancer-derived exosomes are still critical components for preparing the tumor microenvironment by (i) enabling tumor cells to escape from the immunological surveillance and (ii) arranging the pre-metastatic site for the engraftment of detached cancer cells. In this review, we discuss the multifaceted role of EVs in the multiple steps of metastasis. Future research directions draw attention to EVs as biological targets for cancer diagnosis, prognosis and therapy. However, due to their significant role in cell communication, they may become a valuable drug delivery system.

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Extracellular vesicles from MDA-MB-231 breast cancer cells stimulated with linoleic acid promote an EMT-like process in MCF10A cells

Cited by 62 publications

References 51 publications

Extracellular Vesicles in Cancer: Cell-to-Cell Mediators of Metastasis

Extracellular Vesicles in Cancer: Cell-to-Cell Mediators of Metastasis

Extracellular vesicles in the tumor microenvironment: Therapeutic resistance, clinical biomarkers, and targeting strategies

The multifaceted role of extracellular vesicles in metastasis: Priming the soil for seeding

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