Exosome exoWNT3A/RSPO1 mass spectrum data
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Cell Suspension Culture
SUBMITTER: 
Shixiang Wang
LAB HEAD: Yun-Shen Chan
PROVIDER: PXD067589 | Pride | 2025-10-10
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MS_Report_peptide.csv | Csv | |||
| MS_Report_protein.csv | Csv | |||
| MS_exo_3A-RS1_01.raw | Raw | |||
| MS_exo_3A-RS1_02.raw | Raw | |||
| MS_exo_3A-RS1_03.raw | Raw |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:Using human liver progenitor cell cultures, we showed that WNT3A and RSPO1 co-treatment could effectively regulate hepatic cell fate and uncovered their potential functional crosstalk with the PPARα signaling pathway. We also observed that dual ligands loaded on a single exosome (exoWNT3A/RSPO1) hyperactivated the WNT signaling and promoted efficient hepatic organoid growth compared to the small molecule inhibitor CHIR99021. After exoWNT3A/RSPO1 administration, we confirmed the efficient delivery and robust activation of WNT signaling in the mouse liver. Importantly, exoWNT3A/RSPO1 could accelerate liver repair and regeneration under various conditions, including acute and chronic injuries and aging-associated phenotypes.
2025-08-20 | GSE305923 | GEO
Project description:Liver fibrosis is a common pathological process of various chronic liver diseases that can develop into liver cancer. MicroRNAs (miRNAs) are a king of non-coding RNA which are closely related to liver diseases. Thus, this research hope to explore the effect of miR-484 on liver fibrosis and reveal its mechanism. The miRNAs profiles were screened by microRNA sequencing and the location of miR-484 was identified by fluorescence in situ hybridization (FISH) in human liver fibrotic tissues. MiR-484 expression was detected by qRT-PCR in rat primary hepatic stellate cells (HSCs). Bioinformatics analysis and dual-luciferase reporter assay were performed to determine the target gene of miR-484. Liver fibrosis specific signatures were analyzed by qRT-PCR and western blot after miR-484 mimic/inhibitor transfection. The cell apoptosis was detected by Annexin V-FITC/PI double staining. The effect of miR-484 silencing on fibrosis in vivo was investigated in thioacetamide (TAA) induced mice model using the adeno-associated virus carrying miR-484 inhibitor. Enrichment of miR-484 was observed in human liver fibrosis tissues and activated rat primary HSCs. FISH showed that miR-484 was prominently located at fibrotic region and the cytoplasm of HSCs in human liver tissues. Dual-luciferase reporter assay verified that the homeodomain-interacting protein kinases 1 (HIPK1) was the direct target of miR-484. After transfecting miR-484 inhibitor into HSC-T6, HIPK1 were significantly up-regulated, and α-SMA, col1a1, Wnt-3a, Wnt-5a, β-catenin and p-β-catenin were down-regulated, suggesting the restrain effect of miR-484 knockdown on HSCs activation. Conversely, the results were opposite with miR-484 mimic transfection. In addition, the apoptosis of HSC-T6 altered significantly after miR-484 modulation. Moreover, adeno-associated virus carrying miR-484 inhibitor alleviated mice liver fibrosis induced by TAA. In conclusion, miR-484 knockdown ameliorates liver fibrosis by promoting the apoptosis and suppressing HSCs activation via blocking Wnt/β-catenin signaling pathway. MiR-484 and its downstream gene HIPK1 might be selected as novel therapeutic targets of liver fibrosis.
2021-12-09 | GSE190366 | GEO
Project description:Both FGF and WNT pathways play important roles in embryonic development, stem cell self-renewal and are frequently deregulated in breast cancer. To study the cooperation between FGF and WNT signaling, we have generated a mouse model, MMTV-WNT1/MMTV-iFGFR1 (WNT/iR1), in which we could chemically overactivate iFGFR1 in a ligand-independent manner.
2017-11-22 | MSV000081730 | MassIVE
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile duct (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280889 | GEO
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile ducts (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280724 | GEO
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile ducts (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280691 | GEO
Project description:Triple-negative breast cancer (TNBC) initially exhibits a robust response to chemotherapy; however paradoxically, the treatment enriches a population of drug-tolerant persister (DTP) cells, which are known to drive therapy resistance. Therefore, it is crucial to, foremost, identify and subsequently target the signaling pathways implicated in therapy-induced drug resistance and the emergence of DTP cells. In this study, by combining the use of human TNBC cell lines, 3D patient-derived organoid models, and in vivo xenograft models, we identified activation of the Wnt/β-catenin signaling pathway as a common mechanism underlying early DTP cell(s) enrichment in response to different chemotherapeutic agents. Live-cell imaging using Wnt-reporter TNBC cell lines validated diverse patterns of Wnt-transcriptional enrichment, encompassing both intrinsic selection and acquired de novo activation in response to chemotherapy treatment. Purification of differential Wnt-transcriptional populations revealed that post-treatment WntLow cells succumb to apoptosis, while, in contrast, chemotherapy-treated Wnt-active (WntHigh) cells adopt stem cell-like traits, exhibit reduced proliferation, and are, in turn, refractory to treatment. The transition to a post-treatment WntHigh state is orchestrated by increased expression of Wnt ligands, R-spondins, and factors facilitating Wnt ligand secretion, such as PORCN. Consequently, genetic or concomitant - but not sequential - pharmacological inhibition of Wnt ligand secretion alongside chemotherapy prevents treatment-induced WntHigh enrichment and sensitizes TNBC tumors to chemotherapy. Taken together, these observations provide a strong rationale for testing dual treatment comprising chemotherapy and Wnt ligand secretion inhibitors in clinical trials, extending to all TNBC patients.
2025-09-25 | GSE254558 | GEO
Project description:Membrane vesicles released by neoplastic cells into extracellular medium contain potential of carrying arrays of oncogenic molecules including proteins and microRNAs (miRNA). Extracellular (exosome-like) vesicles play a major role in cell-to-cell communication. Thus, the characterization of miRNAs of exosome-like vesicles is imperative in clarifying intercellular signaling as well as identifying disease markers. microarray analysis identified several oncogenic miRNA between the two types vesicles.
2013-11-28 | GSE52802 | GEO
Project description:The most notable progress in renal clear cell carcinoma (ccRCC) in the past decades is the introduction of drugs targeting the VHL-HIF signaling pathway-associated angiogenesis. However, mechanisms underlying the development of VHL mutation-independent ccRCC are unclear. Here we provide evidence that the disrupted Hippo-YAP signaling contributes to the development of ccRCC independent of VHL alteration. We found that YAP1 and its primary target genes are frequently upregulated in ccRCC and the upregulation of these genes is associated with unfavorable patient outcomes. Research results derived from our in vitro and in vivo experimental models demonstrated that, under normoxic conditions, hyperactivated YAP1 drives the expression of FGFs to stimulate the proliferation of tumor and tumor-associated endothelial cells in an autocrine/paracrine manner. When rapidly growing cancer cells create a hypoxic environment, hyperactivated YAP1 in cancer cells induces the production of VEGF, which promotes the angiogenesis of tumor-associated endothelial cells, leading to improved tumor microenvironment and continuous tumor growth. Our study indicates that hyperactivated YAP1 is essential for maintaining a sustainable ccRCC progression, and targeting the dual role of hyperactivated YAP1 represents a novel strategy to improve renal carcinoma therapy.
2025-02-25 | GSE290118 | GEO