Mast cell exosomes promote lung adenocarcinoma cell proliferation ¿ role of KIT-stem cell factor signaling

Xiao, Hui; Lässer, Cecilia; Shelke, Ganesh Vilas; Wang, Juan; Rådinger, Madeleine; Lunavat, Taral R.; Malmhäll, Carina; Lin, Li; Li, Jia; Li, Li; Lötvall, Jan

doi:10.1186/preaccept-1817458803126023

Cited by 28 publications

(34 citation statements)

References 30 publications

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“…Furthermore, the transfer of TrkB may affect recipient cell signalling, since TrkB phosphorylation was upregulated in sh YKL-40 cells treated with pLKO exosomes. A similar mechanism has been reported with c-kit-containing exosomes that activate proliferation and PI3K dependent-signalling pathway [55]. Moreover, TrkB phosphorylation was slightly reduced by treatment of pLKO cells with sh YKL-40 exosomes.…”

Section: Discussionsupporting

confidence: 76%

“…Indeed, inhibition of functional rescue by K252a, a pan-Trk inhibitor [41], inhibiting TrkB activation, suggested that TrkB is implicated in these mechanisms, since TrkA was absent and TrkC was unchanged whatever cell types. TrkB mRNA expression level was unchanged in sh YKL-40 cells suggesting that the increase of TrkB receptor into sh YKL-40 cells is mainly due to its protein transfer through exosomes as already demonstrated with c-kit [55]. Furthermore, the transfer of TrkB may affect recipient cell signalling, since TrkB phosphorylation was upregulated in sh YKL-40 cells treated with pLKO exosomes.…”

Section: Discussionmentioning

confidence: 71%

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TrkB-containing exosomes promote the transfer of glioblastoma aggressiveness to YKL-40-inactivated glioblastoma cells

et al. 2016

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The neurotrophin receptors are known to promote growth and proliferation of glioblastoma cells. Their functions in spreading glioblastoma cell aggressiveness to the microenvironment through exosome release from glioblastoma cells are unknown.Considering previous reports demonstrating that YKL-40 expression is associated with undifferentiated glioblastoma cancer stem cells, we used YKL-40-silenced cells to modulate the U87-MG differentiated state and their biological aggressiveness. Herein, we demonstrated a relationship between neurotrophin-receptors and YKL-40 expression in undifferentiated cells. Differential functions of cells and derived-exosomes were evidenced according to neurotrophin receptor content and differentiated cell state by comparison with control pLKO cells.YKL-40 silencing of glioblastoma cells impairs proliferation, neurosphere formation, and their ability to induce endothelial cell (HBMEC) migration. The modulation of differentiated cell state in YKL-40-silenced cells induces a decrease of TrkB, sortilin and p75NTR cellular expressions, associated with a low-aggressiveness phenotype. Interestingly, TrkB expressed in exosomes derived from control cells was undetectable in exosomes from YKL-40 -silenced cells. The transfer of TrkB-containing exosomes in YKL-40-silenced cells contributed to restore cell proliferation and promote endothelial cell activation. Interestingly, in U87 MG xenografted mice, TrkB-depleted exosomes from YKL-40-silenced cells inhibited tumor growth in vivo.These data highlight that TrkB-containing exosomes play a key role in the control of glioblastoma progression and aggressiveness. Furthermore, TrkB expression was detected in exosomes isolated from plasma of glioblastoma patients, suggesting that this receptor may be considered as a new biomarker for glioblastoma diagnosis.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 71%

TrkB-containing exosomes promote the transfer of glioblastoma aggressiveness to YKL-40-inactivated glioblastoma cells

et al. 2016

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“…Jan Lötvall (University of Gothenburg, Gothenburg, Sweden) reported on an emerging mechanism of micro-environmental cross-talk conducted via exosomes (40–100 nm in diameter) which are secreted by various cell types and play roles in epithelial-to-mesenchymal transition (EMT), tumor hypoxia, cancer invasiveness, metastasis, angiogenesis, and tolerance to chemotherapy (27). …”

Section: Microenvironment Metabolism Inflammation and New Conceptsmentioning

confidence: 99%

Cancer Stem Cells: Targeting the Roots of Cancer, Seeds of Metastasis, and Sources of Therapy Resistance

et al. 2015

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With the goal to remove the roots of cancer, eliminate metastatic seeds, and overcome therapy resistance, the 2014 inaugural International Cancer Stem Cell (CSC) Conference at Cleveland, OH, convened together over 320 investigators, including 55 invited world-class speakers, 25 short oral presenters, and 100 poster presenters, to gain an in-depth understanding of CSCs and explore therapeutic opportunities targeting CSCs. The meeting enabled intriguing discussions on several topics including: genetics and epigenetics; cancer origin and evolution; microenvironment and exosomes; metabolism and inflammation; metastasis and therapy resistance; single cell and heterogeneity; plasticity and reprogramming; as well as other new concepts. Reports of clinical trials targeting CSCs emphasized the urgent need for strategically designing combinational CSC-targeting therapies against cancer.

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“…Tetraspanins, a family of transmembrane proteins (e.g., CD63 and CD81) are among the most abundant surface proteins on exosomes (Booth et al, ; Raposo & Stoorvogel, ) and are often used to quantify total exosome secretion. Exosome release has been demonstrated to increase by induced hypoxia (King, Michael, & Gleadle, ), DNA damage (Lehmann et al, ; Xiao et al, ), and by oxidative stress (Atienzar‐Aroca et al, ). However, not all pathological conditions may induce exosomal secretion.…”

Section: Exosome Release Mechanismsmentioning

confidence: 99%

Exosome release and cargo in Down syndrome

Hamlett

LaRosa

Mufson

et al. 2019

Developmental Neurobiology

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Down syndrome (DS) is a multisystem disorder affecting 1 in 800 births worldwide. Advancing technology, medical treatment, and social intervention have dramatically increased life expectancy, yet there are many etiologies of this disorder that are in need of further research. The advent of the ability to capture extracellular vesicles (EVs) in blood from specific cell types allows for the investigation of novel intracellular processes. Exosomes are one type of EVs that have demonstrated great potential in uncovering new biomarkers of neurodegeneration and disease, and also that appear to be intricately involved in the transsynaptic spread of pathogenic factors underlying Alzheimer's disease and other neurological diseases. Exosomes are nanosized vesicles, generated in endosomal multivesicular bodies (MVBs) and secreted by most cells in the body. Since exosomes are important mediators of intercellular communication and genetic exchange, they have emerged as a major research focus and have revealed novel biological sequelae involved in conditions afflicting the DS population. This review summarizes current knowledge on exosome biology in individuals with DS, both early in life and in aging individuals. Collectively these studies have demonstrated that complex multicellular processes underlying DS etiologies may include abnormal formation and secretion of extracellular vesicles such as exosomes.

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Mast cell exosomes promote lung adenocarcinoma cell proliferation ¿ role of KIT-stem cell factor signaling

Cited by 28 publications

References 30 publications

TrkB-containing exosomes promote the transfer of glioblastoma aggressiveness to YKL-40-inactivated glioblastoma cells

TrkB-containing exosomes promote the transfer of glioblastoma aggressiveness to YKL-40-inactivated glioblastoma cells

Cancer Stem Cells: Targeting the Roots of Cancer, Seeds of Metastasis, and Sources of Therapy Resistance

Exosome release and cargo in Down syndrome

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