ArticleMolecular cancer2024
Myofibroblast-derived extracellular vesicles facilitate cancer stemness of hepatocellular carcinoma via transferring ITGA5 to tumor cells.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Variational sparse Gaussian-process method for detecting spatially variable genes and cellular interactions in spatial transcriptomics.Briefings in bioinformatics · 2026Article
- Improving pancreatic adenocarcinoma prognosis models through ligand receptor interactions and histopathological integration.Journal of translational medicine · 2026Article
- S100A9 Aggravates Cardiac Fibrosis by TLR4/PGC-1α Mediated Macrophage-Myofibroblast Crosstalk.Journal of extracellular vesicles · 2026Article
- A hypoxia-responsive migrasome-related lncRNA signature predicts prognosis and suggests the MSC-AS1/ITGA5 axis as a potential therapeutic target in head and neck squamous cell carcinoma.Functional & integrative genomics · 2026Article
- Extracellular vesicles in solid tumors: from tumor ecology to engineered therapeutics.Molecular cancer · 2026Review
- From bone to beyond: osteoclasts dictate metastatic fate in lung adenocarcinoma via the OLFML3-DPPA2 stemness switch.Biology direct · 2026Article
- Integrins in cancer: insights into mechanisms and therapeutic potential.Cell communication and signaling : CCS · 2026Review
- Ochratoxin A and Clear Cell Renal Cell Carcinoma: Exploring Potential Molecular Links Through Network Toxicology and Machine Learning.International journal of molecular sciences · 2026Article
- The mitochondrial translocation of phosphorylated EZH2 promotes PARP inhibitor resistance in BRCA1-deficient epithelial ovarian cancer.Cell discovery · 2026Article
- Obesity- and tumor-derived signals drive cancer-associated state transitions in breast mesenchymal stromal/stem cells reprogrammed by IL1RA or JAK inhibition.Experimental hematology & oncology · 2026Article
- Role and mechanism of miR‑222‑5p in endothelial cell apoptosis.Molecular medicine reports · 2026Article
- Smoking-Induced STC2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Engineered cyclic peptide targeting ITGA5 disrupts tumor-stroma interaction to overcome desmoplasia and resistance in pancreatic ductal adenocarcinoma.Acta pharmaceutica Sinica. B · 2026Article
- Identification of a migrasome-related lncRNA signature and its prognostic and immunological role in bladder cancer.Frontiers in immunology · 2026Article
- Thermoradiotherapy reverses proliferation, metastasis, and anoikis resistance in glioblastoma through ITGA5-PI3K/AKT axis.Translational oncology · 2025Article
- Whole-genome methylation profiling of extracellular vesicle DNA in gastric cancer identifies intercellular communication features.Nature communications · 2025Article
- Article
- ITGA5 promotes cervical cancer progression by regulating IMP3 recruitment of HK2 mRNA.American journal of translational research · 2025Article
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12 authors.
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Abstract
backgroundMyofibroblasts constitute a significant component of the tumor microenvironment (TME) and play a pivotal role in the progression of hepatocellular carcinoma (HCC). Integrin α5 (ITGA5) is a crucial regulator in myofibroblasts of malignant tumors. Therefore, the potential of ITGA5 as a novel target for the therapeutic strategy of HCC should be investigated.
methodsDigital scanning and analysis of the HCC tissue microarray were performed to locate the distribution of ITGA5 and conduct the prognosis analysis. CRISPR Cas9-mediated ITGA5 knockout was performed to establish the ITGA5-KO myofibroblast cell line. Extracellular vesicles (EVs) derived from LX2 were extracted for the treatment of HCC cells. Subsequently, the sphere-forming ability and the stemness markers expression of the treated HCC cells were examined. An orthotopic HCC mouse model with fibrotic injury was constructed to test the outcomes of ITGA5-targeting therapy and its efficacy in the programmed death-ligand 1 (PD-L1) treatment. Co-immunoprecipitation/mass spectrometry and transcriptome data were integrated to delve into the mechanism.
resultsThe tissue microarray results revealed that ITGA5 was highly enriched in the stromal myofibroblasts of HCC tissues and contributed to enhanced tumor progression and poor prognosis. Notably, ITGA5 transmission via extracellular vesicles (EVs) from myofibroblasts to HCC cells induced the acquisition of cancer stem cell-like properties. Mechanistically, ITGA5 directly bind to YES1, facilitating the activation of YES1 and its downstream pathways, thereby enhancing the stemness of HCC cells. Furthermore, the blockade of ITGA5 impeded tumor progression driven by ITGA5
conclusionsOur findings elucidated a novel mechanism by which the EV-mediated transfer of ITGA5 from myofibroblasts to tumor cells augmented HCC stemness. ITGA5-targeting therapy helped prevent the progression of HCC and improved the efficacy of PD-L1 treatment.
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