Similar Datasets
Project description:Transmission of extracellular vesicle packaged lncRNA from TAMs to breast cancer cells
| PRJNA473556 | ENA
Project description:Extracellular vesicle‑packaged microRNAs (miRNAs) are a class of circulating miRNAs located in the plasma that are packaged into extracellular vesicles. The present study examined the expression profiles of extracellular vesicles and tissue miRNAs with the aim of investigating the miRNA signatures in early‑stage breast cancer. The present study identified and compared the extracellular vesicle‑packaged miRNA expression signature and tissue miRNA expression signature from healthy individuals (n=10) and patients with early‑stage breast cancer (n=12). A total of five miRNAs, including miRNA‑375, miRNA‑24‑2‑5p, miRNA‑548b‑5p, miRNA‑655‑3P and miRNA‑376b‑5p, were synchronized in extracellular vesicles and tissues of the breast cancer group when compared with the healthy group. The highest area under the curve (AUC) for a single miRNA was achieved with miRNA‑548b‑5p [AUC=0.785; 95% confidence interval (CI)=0.585‑0.984; P=0.022]. The highest overall AUC was achieved by the combination of miRNA‑375, miRNA‑655‑3p, miRNA‑548b‑5p and miRNA‑24‑2‑5p (AUC=0.808; 95% CI=0.629‑0.986; P=0.013). The Kaplan‑Meier curves and log test analysis results of these five miRNAs, especially those for miRNA‑548b‑5p, were partly consistent with the hypothesis. Two miRNAs (miRNA‑548b‑5p and miRNA‑376b‑5p) were positively associated with patient survival, while two miRNAs (miRNA‑375 and miRNA‑24‑2‑5p) were negatively associated with patient survival. The present study provided a set of plasma extracellular vesicle‑packaged miRNA‑based biomarkers for the diagnosis of early‑stage breast cancer.
| S-EPMC6797958 | biostudies-literature
Project description:We compared the circRNA expression profiles of TAMs versus MDMs, EVs from TAMs versus those from MDMs and Hep3B cells co-cultured with TAMs versus those cultured alone.
2024-08-29 | GSE241868 | GEO
Project description:Small ubiquitin-like modifier (SUMO) binding (termed SUMOylation) emerged as the inducer for the sorting of bioactive molecules into extracellular vesicles (EVs), triggering lymphangiogenesis and further driving tumor lymph node (LN) metastasis, but the precise mechanisms remain largely unclear. Here, we show that bladder cancer (BCa) cell-secreted EVs mediated intercellular communication with human lymphatic endothelial cells (HLECs) through transmission of the long noncoding RNA ELNAT1 and promoted lymphangiogenesis and LN metastasis in a SUMOylation-dependent manner in both cultured BCa cell lines and mouse models. Mechanistically, ELNAT1 induced UBC9 overexpression to catalyze the SUMOylation of hnRNPA1 at the lysine 113 residue, which mediated recognition of ELNAT1 by the endosomal sorting complex required for transport (ESCRT) and facilitated its packaging into EVs. EV-mediated ELNAT1 was specifically transmitted into HLECs and epigenetically activated SOX18 transcription to induce lymphangiogenesis. Importantly, blocking the SUMOylation of tumor cells by downregulating UBC9 expression markedly reduced lymphatic metastasis in EV-mediated, ELNAT1-treated BCa in vivo. Clinically, EV-mediated ELNAT1 was correlated with LN metastasis and a poor prognosis for patients with BCa. These findings highlight a molecular mechanism whereby the EV-mediated ELNAT1/UBC9/SOX18 regulatory axis promotes lymphangiogenesis and LN metastasis in BCa in a SUMOylation-dependent manner and implicate ELNAT1 as an attractive therapeutic target for LN metastatic BCa.
| S-EPMC8262506 | biostudies-literature
Project description:Circulating extracellular vesicle (EV)-derived microRNAs (miRNAs) are now considered the next generation of cancer "theranostic" tools, with strong clinical relevance. Although their potential in breast cancer diagnosis has been widely reported, further studies are still required to address this challenging issue. The present study examined the expression profiles of EV-packaged miRNAs to identify novel miRNA signatures in breast cancer and verified their diagnostic accuracy. Circulating EVs were isolated from healthy controls and breast cancer patients and characterized following the MISEV 2018 guidelines. RNA-sequencing and real-time PCR showed that miRNA-27a and miRNA-128 were significantly down-regulated in patient-derived EVs compared to controls in screening and validation cohorts. Bioinformatics analyses of miRNA-target genes indicated several enriched biological processes/pathways related to breast cancer. Receiver operating characteristic (ROC) curves highlighted the ability of these EV-miRNAs to distinguish breast cancer patients from non-cancer controls. According to other reports, the levels of EV-miRNA-27a and EV-miRNA-128 are not associated with their circulating ones. Finally, evidence from the studies included in our systematic review underscores how the expression of these miRNAs in biofluids is still underinvestigated. Our findings unraveled the role of serum EV-derived miRNA-27a and miRNA-128 in breast cancer, encouraging further investigation of these two miRNAs within EVs towards improved breast cancer detection.
| S-EPMC10649351 | biostudies-literature
Project description:Cancer-derived extracellular vesicles are known to play a role in the progression of the disease. In this rapidly-growing field, there are many reports of phenotypic changes in cells following exposure to cancer-derived extracellular vesicles. This study examines the protein contents of vesicles derived from three well-known breast cancer cell lines, MCF-7, MDA-MB-231 and T47D, using peptide-centric LC-MS/MS and cytokine multiplex immunoassay analysis to understand the molecular basis of these changes. Through these techniques a large number of proteins within these vesicles were identified. A large proportion of these proteins are known to be important in cancer formation and progression and associated with cancer signaling, angiogenesis, metastasis and invasion and immune regulation. This highlights the importance of extracellular vesicles (EVs) in cancer communications and shows some of the mechanisms the vesicles use to assist in cancer progression.
| S-EPMC7403963 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-08 | GSE127872 | GEO
Project description:Purpose: Extracellular vesicle (EV)‑derived microRNAs (miRNAs) are a class of circulating miRNAs located in the plasma that are are now considered the next generation of cancer “theranostic” tools, with a strong clinical relevance. Although the potential role of EV-packaged miRNAs in breast cancer diagnosis has been widely reported, further studies are still demanded to address this challenging issue. The present study examined the expression profiles of EVs and circulating miRNAs with the aim of identifying novel miRNA signatures in breast cancer, and verify their diagnostic accurancy.
2023-12-06 | GSE239341 | GEO
Project description:Progressive peritoneal fibrosis and the loss of peritoneal function often emerged in patients undergoing long-term peritoneal dialysis (PD), resulting in PD therapy failure. Varieties of cell-cell communications among peritoneal cells play a significant role in peritoneal fibrogenesis. Extracellular vesicles (EVs) have been confirmed to involve in intercellular communication by transmitting proteins, nucleic acids or lipids. However, their roles and functional mechanisms in peritoneal fibrosis remain to be determined. Using integrative analysis of EV proteomics and single-cell RNA sequencing, we characterized the EVs isolated from PD patient's effluent and revealed that mesothelial cells are the main source of EVs in PD effluent. We demonstrated that transforming growth factor-β1 (TGF-β1) can substitute for PD fluid to stimulate mesothelial cells releasing EVs, which in turn promoted fibroblast activation and peritoneal fibrogenesis. Blockade of EVs secretion by GW4869 or Rab27a knockdown markedly suppressed PD-induced fibroblast activation and peritoneal fibrosis. Mechanistically, injured mesothelial cells produced EVs containing high level of integrin-linked kinase (ILK), which was delivered to fibroblast and activated them via p38 MAPK signalling pathway. Clinically, the expression of ILK was up-regulated in fibrotic peritoneum of patients undergoing long-term PD. The percentage of ILK positive EVs in PD effluent correlated with peritoneal dysfunction and the degree of peritoneal damage. Our study highlights that peritoneal EVs mediate communications between mesothelial cells and fibroblasts to initiate peritoneal fibrogenesis. Targeting EVs or ILK could provide a novel therapeutic strategy to combat peritoneal fibrosis.
| S-EPMC10291285 | biostudies-literature
Project description:Mounting evidence suggests that extracellular vesicles (EVs) are effective communicators in biological signalling in cardiac physiology and pathology. However, the role of EVs in cardiac injury, particularly in ischemic myocardial scenarios, has not been fully elucidated. Here, we report that acute myocardial infarction (AMI)-induced EVs can impair cardiomyocyte survival and exacerbate cardiac injury. EV-encapsulated miR-503, which is enriched during the early phase of AMI, is a critical molecule that mediates myocardial injury. Functional studies revealed that miR-503 promoted cardiomyocyte death by directly binding to peroxisome proliferator-activated receptor gamma coactivator-1β (PGC-1β) and a mitochondrial deacetylase, sirtuin 3 (SIRT3), thereby triggering mitochondrial metabolic dysfunction and cardiomyocyte death. Mechanistically, we identified endothelial cells as the primary source of miR-503 in EVs after AMI. Hypoxia induced rapid H3K4 methylation of the promoter of the methyltransferase-like 3 gene (METTL3) and resulted in its overexpression. METTL3 overexpression evokes N6-methyladenosine (m6 A)-dependent miR-503 biogenesis in endothelial cells. In summary, this study highlights a novel endogenous mechanism wherein EVs aggravate myocardial injury during the onset of AMI via endothelial cell-secreted miR-503 shuttling.
| S-EPMC9028097 | biostudies-literature