Bibliometric and visualized analysis of global research on microRNAs in gastric cancer: from 2013 to 2023.

Gastric cancer (GC) imposes a heavy burden on global public health, and microRNAs (miRNAs) play a crucial role in the diagnosis and treatment of GC. Therefore, it is necessary to clarify the hotspots and frontiers in the field of miRNAs in GC to guide future research. A total of 2,051 publications related to miRNAs in GC from January 2013 to December 2023 were searched from the Web of Science Core Collection database. CiteSpace was used to identify research hotspots and delineate developmental trends. In the past decade, China, Nanjing Medical University, and Ba Yi were the most contributing research country, institute, and author in this field, respectively. The role of miRNAs as biomarkers in GC, the mechanism of miRNAs in the progression of GC, and the impact of the mutual effects between miRNAs and Helicobacter pylori on GC have been regarded as the research hotspots. The mechanisms of miRNAs on glucose metabolism and the application of the roles of circular RNAs as miRNA sponges in GC treatment will likely be frontiers. Overall, this study called for strengthened cooperation to identify targets and therapeutic regimes for local specificity and high-risk GC types, and to promote the translation of research results into clinical practice.

Identification of Key Genes and Pathways in Oxaliplatin-Induced Neuropathic Pain Through Bioinformatic Analysis.

Background: The mechanism of Chemotherapy-induced neuropathic pain (NP) remains obscure. This study was aimed to uncover the key genes as well as protein networks that contribute to Oxaliplatin-induced NP. Material/Methods: Oxaliplatin frequently results in a type of Chemotherapy-induced NP that is marked by heightened sensitivity to mechanical and cold stimuli, which can lead to intolerance and discontinuation of medication. We investigated whether these different etiologies lead to similar pathological outcomes by targeting shared genetic targets or signaling pathways. Gene expression data were obtained from the Gene Expression Comprehensive Database (GEO) for GSE38038 (representing differential expression in the spinal nerve ligation model rats) and GSE126773 (representing differential expression among the Oxaliplatin-induced NP model rats). Differential gene expression analysis was performed using GEO2R. Results: Protein-protein interaction (PPI) analysis identified 260 co-differentially expressed genes (co-DEGs). Subsequently, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed three shared pathways involved in both models: Kaposi sarcoma-associated herpesvirus (KSHV) infection, Epstein-Barr virus (EBV) infection, and AGE-RAGE signaling pathway in diabetic complications. Further bioinformatics analysis highlighted eight significantly up-regulated genes in the NP group: Mapk14, Icam1, Cd44, IL6, Cxcr4, Stat1, Casp3 and Fgf2. Our results suggest that immune dysfunction, inflammation-related factors or regulating inflammation factors may also be related to Oxaliplatin-induced NP. Additionally, we analyzed a dataset (GSE145222) involving chronic compression of DRGs (CCD) and control groups. CCD model is a classic model for studying NP. We assessed these hub genes' expression levels. In contrast with the control groups, the hub genes were up-regulated in CCD groups, the difference was statistically significant, except Stat1. Conclusion: Our research significantly contributes to elucidating the mechanisms underlying the occurrence as well as the progression of Oxaliplatin-induced NP. We have identified crucial genes and signaling pathways associated with this condition.

The relationship between lactate dehydrogenase and Apolipoprotein A1 levels in patients with severe pneumonia.

Background: To investigate the relationship between lactate dehydrogenase and apolipoprotein A1 levels and the condition and prognosis of patients with severe pneumonia. Methods: Data was collected from 204 patients with severe pneumonia who were hospitalized from January 1, 2019 to December 1, 2021 in Zhaotong First People's Hospital (respiratory intensive care unit (RICU)), and divided into survival group (160 patients) and death group (44 patients) according to their hospitalization outcome. The relationship between lactate dehydrogenase and apolipoprotein A1 levels and general information, disease, and treatment needs of patients with severe pneumonia was analyzed, and lactate dehydrogenase, apolipoprotein A1, neutrophil-to-lymphocyte ratio, hematocrit, C-reactive protein, calcitoninogen, D-dimer, Acute Physiology and Chronic Health Status Rating System II, and Pneumonia Severity Index scores were compared between the survival and death groups. The value of these indicators in determining the prognosis of patients was analyzed using subject operating characteristic (ROC) curves. Logistic regression was used to analyze the risk factors for death from severe pneumonia.

circRNAs as prognostic markers in pediatric acute myeloid leukemia.

Circular RNAs (circRNAs) arise from precursor mRNA processing through back-splicing and have been increasingly recognized for their functions in various cancers including acute myeloid leukemia (AML). However, the prognostic implications of circRNA in AML remain unclear. We conducted a comprehensive genome-wide analysis of circRNAs using RNA-seq data in pediatric AML. We revealed a group of circRNAs associated with inferior outcomes, exerting effects on cancer-related pathways. Several of these circRNAs were transcribed directly from genes with established functions in AML, such as circRUNX1, circWHSC1, and circFLT3. Further investigations indicated the increased number of circRNAs and linear RNAs splicing were significantly correlated with inferior clinical outcomes, highlighting the pivotal role of splicing dysregulation. Subsequent analysis identified a group of upregulated RNA binding proteins in AMLs associated with high number of circRNAs, with TROVE2 being a prominent candidate, suggesting their involvement in circRNA associated prognosis. Through the integration of drug sensitivity data, we pinpointed 25 drugs that could target high-risk AMLs characterized by aberrant circRNA transcription. These findings underscore prognostic significance of circRNAs in pediatric AML and offer an alternative perspective for treating high-risk cases in this malignancy.

Novel Zn0.079V2O5·0.53H2O/Graphene aerogel as high-rate and long-life cathode materials of aqueous zinc-ion batteries.

Aqueous zinc-ion batteries (ZIBs) have attracted more and more attention due to their advantages of low cost, high safety and environmental protection. Unfortunately, the unsatisfactory capacity at high current density and long-term cycling performance of cathode materials hinder the development of ZIBs. Here, a novel Zn0.079V2O5·0.53H2O/graphene (ZVOH@rGO) hybrid aerogel composed of ultrathin Zn0.079V2O5·0.53H2O (ZVOH) nanoribbons and 3D continuous graphene conductive network was successfully prepared and used as cathode of ZIBs. Taking advantage of the synergistic effects associated with ion doping, morphology control and unique aerogel structure, the ZVOH@rGO electrode demonstrated ultrafast charge/discharge capability and remarkable cycling stability: A high reversible capacity of 286.7 mAh g-1 was achieved at a current density as large as 30 A g-1, and an impressive capacity retention ratio of 75.6 % was realized over 9800 ultra-long cycles at 12 A g-1. This work is of great significance for the synthesis modification of vanadium oxides and the development of high performance ultrafast charge-discharge ZIBs.

Catalyzing Desolvation at Cathode-Electrolyte Interface Enabling High-Performance Magnesium-Ion Batteries.

Magnesium ion batteries (MIBs) are expected to be the promising candidates in the post-lithium-ion era with high safety, low cost and almost dendrite-free nature. However, the sluggish diffusion kinetics and strong solvation capability of the strongly polarized Mg2+ are seriously limiting the specific capacity and lifespan of MIBs. In this work, catalytic desolvation is introduced into MIBs for the first time by modifying vanadium pentoxide (V2 O5 ) with molybdenum disulfide quantum dots (MQDs), and it is demonstrated via density function theory (DFT) calculations that MQDs can effectively lower the desolvation energy barrier of Mg2+ , and therefore catalyze the dissociation of Mg2+ -1,2-Dimethoxyethane (Mg2+ -DME) bonds and release free electrolyte cations, finally contributing to a fast diffusion kinetics within the cathode. Meanwhile, the local interlayer expansion can also increase the layer spacing of V2 O5 and speed up the magnesiation/demagnesiation kinetics. Benefiting from the structural configuration, MIBs exhibit superb reversible capacity (≈300 mAh g-1 at 50 mA g-1 ) and unparalleled cycling stability (15 000 cycles at 2 A g-1 with a capacity of ≈70 mAh g-1 ). This approach based on catalytic reactions to regulate the desolvation behavior of the whole interface provides a new idea and reference for the development of high-performance MIBs.

Synthesis, Bioactivities, and Antibacterial Mechanism of 5-(Thioether)-N-phenyl/benzyl-1,3,4-oxadiazole-2-carboxamide/amine Derivatives.

1,3,4-Oxadiazole thioethers have shown exciting antibacterial activities; however, the current mechanism of action involving such substances against bacteria is limited to proteomics-mediated protein pathways and differentially expressed gene analysis. Herein, we report a series of novel 1,3,4-oxadiazole thioethers containing a carboxamide/amine moiety, most of which show good in vitro and in vivo bacteriostatic activities. Compounds A10 and A18 were screened through CoMFA models as optimums against Xanthomonas oryzae pv. oryzae (Xoo, EC50 values of 5.32 and 4.63 mg/L, respectively) and Xanthomonas oryzae pv. oryzicola (Xoc, EC50 values of 7.58 and 7.65 mg/L, respectively). Compound A10 was implemented in proteomic techniques and activity-based protein profiling (ABPP) analysis to elucidate the antibacterial mechanism and biochemical targets. The results indicate that A10 disrupts the growth and pathogenicity of Xoc by interfering with pathways associated with bacterial virulence, including the two-component regulation system, flagellar assembly, bacterial secretion system, quorum sensing, ABC transporters, and bacterial chemotaxis. Specifically, the translational regulator (CsrA) and the virulence regulator (Xoc3530) are two effective target proteins of A10. Knocking out the CsrA or Xoc3530 gene in Xoc results in a significant reduction in the motility and pathogenicity of the mutant strains. This study contributes available molecular entities, effective targets, and mechanism basis for the management of rice bacterial diseases.

Exosome-derived tRNA fragments tRF-GluCTC-0005 promotes pancreatic cancer liver metastasis by activating hepatic stellate cells.

Early metastasis is the primary factor in the very poor prognosis of pancreatic ductal adenocarcinoma (PDAC), with liver metastasis being the most common form of distant metastasis in PDAC. To investigate the mechanism of PDAC liver metastasis, we found that PDAC cells can promote the formation of pre-metastatic niches (PMNs) through exosomes to facilitate liver metastasis in the early stage. In our study, hepatic stellate cells (HSCs) were treated with PDAC-derived exosomes (PDAC-exo), and the activation of HSCs was detected. A novel transfer RNA-derived fragment, the tRF-GluCTC-0005 was obtained by small RNA sequencing from serum exosomes of PDAC patients. Bioinformatics analysis and RNA pull-down assays revealed the interaction between WDR1 and tRF-GluCTC-0005. A KPC transgenic mouse model and an AAV-mediated sh-WDR1 mouse model were used to detect the mechanism of liver metastasis in vivo. Finally, the dual luciferase reporter assay, protein mutation truncation assay, Co-IP assay, and flow cytometry assay were used to explore the molecular mechanism in HSCs activation and PMNs formation. We found that the tRF-GluCTC-0005 in exosomes binds to the 3' untranslated region of the mRNA of the WDRl in HSCs and increases mRNA stability. The N-terminals of WDR1 bind to the YAP protein directly, inhibit YAP phosphorylation, and promote the expression of YAP transcription factors. The tRF-GluCTC-0005 in PDAC-exo significantly recruits myeloid-derived suppressor cells (MDSCs) in the liver, creating a PMNs immunosuppressive microenvironment and further advancing liver metastasis from PDAC. Our results suggest that the key of PDAC liver metastasis is the activation of HSCs through upregulation of WDR1 by tRF-GluCTC-0005 in exosomes, which mediates the infiltration of MDSCs to form PMNs.

Can CT-Based Arterial and Venous Morphological Markers of Chronic Obstructive Pulmonary Disease Explain Pulmonary Vascular Remodeling?

RATIONALE AND OBJECTIVES: We analyzed changes in quantitative pulmonary artery and vein parameters to investigate pulmonary vascular remodeling characteristics in chronic obstructive pulmonary disease (COPD) patients. MATERIALS AND METHODS: This retrospective study recruited healthy volunteers and COPD patients. Participants undergoing standard-of-care pulmonary function testing (PFT) and computed tomography (CT) evaluations were classified into five groups: normal and Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades 1-4. Artery and vein analyses (volumes, numbers, densities, and fractions) were performed using artificial intelligence. RESULTS: Among 139 subjects (136 men; mean age, 64years±8 [SD]) with GOLD grade 1 (n = 13), grade 2 (n = 49), grade 3 (n = 42), grade 4 (n = 17) and control subjects (n = 18) enrolled, differences in arterial volumes (BV5-10, BV10+, pulmonary arterial volume) and venous densities (BV5 density, BV10+ density, pulmonary venous density, pulmonary venous branch density) among control and GOLD grades 1-4 were statistically significant (P < .05). Higher pulmonary arterial volumes and lower number were observed with more advanced COPD. The number and volumes of pulmonary veins were lower in GOLD grades 2 and 3 than in GOLD grade 1 but higher in GOLD grade 4 than in GOLD grade 3. The numbers and volumes of pulmonary arteries and veins showed varying positive correlations (γ = 0.18-0.96, P < .05). Pulmonary vascular densities were mildly to moderately correlated with PFT results (γ = 0.236-0.495, P < .05) and were moderately negatively correlated with the emphysema percentage (γ = -0.591 to -0.315, P < .05). CONCLUSION: Patients with COPD exhibited pulmonary vascular remodeling, which occurred in the arteries at the early grade of COPD and in the veins at the late grade. CT-based quantitative analysis of pulmonary vasculature may become an imaging marker for early diagnosis and assessment of COPD severity.

Bactericidal bissulfone B7 targets bacterial pyruvate kinase to impair bacterial biology and pathogenicity in plants.

The prevention and control of rice bacterial leaf blight (BLB) disease has not yet been achieved due to the lack of effective agrochemicals and available targets. Herein, we develop a series of novel bissulfones and a novel target with a unique mechanism to address this challenge. The developed bissulfones can control Xanthomonas oryzae pv. oryzae (Xoo), and 2-(bis(methylsulfonyl)methylene)-N-(4-chlorophenyl) hydrazine-1-carboxamide (B7) is more effective than the commercial drugs thiodiazole copper (TC) and bismerthiazol (BT). Pyruvate kinase (PYK) in Xoo has been identified for the first time as the target protein of our bissulfone B7. PYK modulates bacterial virulence via a CRP-like protein (Clp)/two-component system regulatory protein (regR) axis. The elucidation of this pathway facilitates the use of B7 to reduce PYK expression at the transcriptional level, block PYK activity at the protein level, and impair the interaction within the PYK-Clp-regR complex via competitive inhibition, thereby attenuating bacterial biology and pathogenicity. This study offers insights into the molecular and mechanistic aspects underlying anti-Xoo strategies that target PYK. We believe that these valuable discoveries will be used for bacterial disease control in the future.

p-Cresol-Enabled Nickel-Catalyzed Intermolecular Redox-Economical Coupling of Allyl Alcohols with Alkynes through oxa-Nickelacycle.

An intermolecular redox-economical coupling reaction of allyl alcohols with alkynes, catalyzed by Ni-Brønsted acid cocatalysis, has been developed. This method allows for the synthesis of a diverse range of γ,δ-unsaturated ketones with yields ranging from 40% to 94%, while maintaining excellent compatibility with various functional groups. The transformation of the resulting product demonstrates the significant practical value of this method. Further mechanistic investigations have revealed that the reaction proceeds through the formation of an oxa-nickelacycle intermediate.

Intermolecular Carbophosphination of Alkynes with Phosphole Oxides via Ni-Al Bimetal-Catalyzed C-P Bond Activation.

Intermolecular carbophosphination reaction of alkynes or alkenes with unreactive C-P bonds remains an elusive challenge. Herein, we used a Ni-Al bimetallic catalyst to realize an intermolecular carbophosphination reaction of alkynes with 5-membered phosphole oxides, providing a series of 7-membered phosphepines in up to 94 % yield.

Chromatin accessibility landscape of relapsed pediatric B-lineage acute lymphoblastic leukemia.

For around half of the pediatric B-lineage acute lymphoblastic leukemia (B-ALL) patients, the molecular mechanism of relapse remains unclear. To fill this gap in knowledge, here we characterize the chromatin accessibility landscape in pediatric relapsed B-ALL. We observe rewired accessible chromatin regions (ACRs) associated with transcription dysregulation in leukemia cells as compared with normal B-cell progenitors. We show that over a quarter of the ACRs in B-ALL are in quiescent regions with high heterogeneity among B-ALLs. We identify subtype-specific and allele-imbalanced chromatin accessibility by integrating multi-omics data. By characterizing the differential ACRs between diagnosis and relapse in B-ALL, we identify alterations in chromatin accessibility during drug treatment. Further analysis of ACRs associated with relapse free survival leads to the identification of a subgroup of B-ALL which show early relapse. These data provide an advanced and integrative portrait of the importance of chromatin accessibility alterations in tumorigenesis and drug responses.

Abnormal expression of CXCL13, MIF and IL-35 in patients with primary Sjögren's syndrome and its relationship with disease severity.

Introduction: The aim of the study was to detect the saliva chemokine (C-X-C motif) ligand 13 (CXCL13), macrophage migration inhibitory factor (MIF), and interleukin 35 (IL-35) levels in patients with primary Sjögren's syndrome (pSS) and pSS-associated interstitial lung disease (pSS-ILD), and to explore the relationship between CXCL13, MIF, IL-35 levels, and disease severity. Material and methods: ESSDAI score was used to evaluate the disease activity of pSS patients, and the levels of CXCL13, MIF and IL-35 in saliva of subjects were detected and analyzed, and the relationship between CXCL13, MIF, IL-35 and the occurrence of pSS was evaluated. Pearson's correlation coefficient was used to analyze the correlation between CXCL13, MIF, IL-35 and ESSDAI score. ROC curve analysis was conducted to assess the diagnostic value of CXCL13, MIF, IL-35 and their combined application in pSS. Results: The levels of CXCL13, MIF, and IL-35 in saliva were positively correlated with ESSDAI score. Saliva CXCL13 and IL-35 are risk factors for the development of pSS into pSS-ILD. The ROC curve shows that the combination of saliva CXCL13, MIF and IL-35 has the highest diagnostic efficiency for pSS-ILD. Conclusions: CXCL13, MIF and IL-35 are related to the activity of pSS, and the combined diagnosis of these three indexes is expected to be an important method to predict the occurrence and development of pSS.

Association analysis of agronomic traits and construction of genetic networks by resequencing of 306 sugar beet (Beta vulgaris L.) lines.

Due to the relatively brief domestication history of sugar beet (Beta vulgaris ssp. vulgaris), our understanding of the genomic diversity and functional genes in its cultivars is limited, resulting in slow breeding progress. To address this issue, a total of 306 germplasm materials of major cultivars and breeding lines from China, the USA, and Europe were selected for genome resequencing. We investigated population structure and genetic diversity and performed selective scanning of genomic regions, identifying six novel genes associated with important agronomic traits: the candidate genes DFAX2 and P5CS for skin roughness; the candidate genes FRO5, GL24, and PPR91 for root yield and sugar yield, and the pleiotropic candidate gene POLX for flourishing growth vigour, plant height, crown size, flesh coarseness, and sugar yield. In addition, we constructed a protein-protein interaction network map and a phenotype-gene network map, which provide valuable information for identifying and characterizing functional genes affecting agronomic traits in sugar beet. Overall, our study sheds light on the future improvement of sugar beet agronomic traits at the molecular level.

Retraction notice to "Estimation of aboveground biomass of vegetation based on Landsat 8 OLI images" [Heliyon 8, 2022 Article e11099].

[This retracts the article DOI: 10.1016/j.heliyon.2022.e11099.].

Enabling Ultrafast Single Mg2+ Insertion Kinetics of Magnesium-Ion Batteries via In Situ Dynamic Catalysis and Re-equilibration Effects.

Magnesium-ion batteries (MIBs) have great potential in large-scale energy storage field with high capacity, excellent safety, and low cost. However, the strong solvation effect of Mg2+ will lead to the formation of solvated ions in electrolytes with larger size and sluggish diffusion/reaction kinetics. Here, the concept of interfacial catalytic bond breaking is first introduced into the cathode design of MIBs by hybriding MoS2 quantum dots with VS4 (VS4@MQDs) as the cathode. The "in situ dynamic catalysis and re-equilibration" effects can catalyze the Cl-Mg bond breaking and trigger single Mg2+ insertion/extraction chemistries, which can significantly accelerate the diffusion and reaction kinetics, as verified by the decreased diffusion energy barriers (0.26 eV for Mg2+ vs 2.47 eV for MgCl+) and fast diffusion coefficient. Benefitting from these dynamic catalysis effects, the constructed VS4@MQD-based MIBs deliver a high discharge capacity of ∼120 mA h g-1 at 200 mA g-1 and a long-term cyclic stability of 1000 cycles at 1 A g-1. The improved performance and detailed characterizations well prove that the active ions in MIBs change from MgCl+/Mg2Cl3+ to Mg2+ with fast kinetics.

Lariciresinol protects rats from complete Freund's adjuvant induced arthritis in rats via modulation of transforming growth factor-ß and nuclear factor kappa B pathway: An in vivo and in silico study.

Rheumatoid arthritis (RA) is a severe inflammatory auto-immune disorder affecting millions of people across the globe. The current therapeutic options are not adequate to address the complications of RA. Therefore, the present study was conducted to elucidate the protective effect of lariciresinol, a lignan, against Complete Freund's adjuvant (CFA)-induced arthritis in rats. The results of the study showed that lariciresinol improves paw swelling and arthritic scores in rats as compared to CFA rats. Lariciresinol also showed a significant reduction in rheumatoid factor, C-reactive protein, tumor necrosis factor-α, interleukin (IL)-17, and tissue inhibitor of metalloproteinases-3 level with a simultaneous increase in IL-4 level. The burden of oxidative stress was also reduced in CFA rats, as shown by reduced MDA levels and increased SOD and GPx after the administration of lariciresinol. In a Western blot analysis, lariciresinol showed a significant reduction of transforming growth factor-ß and nuclear factor-κB (NF-κB) protein levels in CFA rats. To understand the binding characteristic of lariciresinol with NF-κB, molecular docking analysis was conducted, which showed Larciresinol interacted with the active site of NF-κB. Our study demonstrated the significant protective effect of lariciresinol against RA via multi-target action.

The stromal-tumor amplifying STC1-Notch1 feedforward signal promotes the stemness of hepatocellular carcinoma.

BACKGROUND: Cancer-associated fibroblasts (CAFs), an important component of the tumor microenvironment (TME), play crucial roles in tumor stemness. It has been shown in various cancer studies that stanniocalcin-1 (STC1) is secreted by CAFs, however, its function in HCC is still not clear. METHODS: The serum concentration and intracellular expression level of STC1 were quantified by ELISA and western blotting, respectively. The role of CAF-derived STC1 in HCC stemness was investigated by sphere formation, sorafenib resistance, colony formation, and transwell migration and invasion assays in vitro and in an orthotopic liver xenograft model in vivo. An HCC tissue microarray containing 72 samples was used to evaluate the expression of STC1 and Notch1 in HCC tissues. Coimmunoprecipitation (CoIP) and dual-luciferase reporter assays were performed to further explore the underlying mechanisms. ELISAs were used to measure the serum concentration of STC1 in HCC patients. RESULTS: We demonstrated that CAFs were the main source of STC1 in HCC and that CAF-derived STC1 promoted HCC stemness through activation of the Notch signaling pathway. In HCC patients, the expression of STC1 was positively correlated with Notch1 expression and poor prognosis. The co-IP assay showed that STC1 directly bound to Notch1 receptors to activate the Notch signaling pathway, thereby promoting the stemness of HCC cells. Our data further demonstrated that STC1 was a direct transcriptional target of CSL in HCC cells. Furthermore, ELISA revealed that the serum STC1 concentration was higher in patients with advanced liver cancer than in patients with early liver cancer. CONCLUSIONS: CAF-derived STC1 promoted HCC stemness via the Notch1 signaling pathway. STC1 might serve as a potential biomarker for the prognostic assessment of HCC, and the stromal-tumor amplifying STC1-Notch1 feedforward signal could constitute an effective therapeutic target for HCC patients.

An exosome-related lncRNA signature correlates with prognosis, immune microenvironment, and therapeutic responses in hepatocellular carcinoma.

BACKGROUND: Exosomes act as essential modulators of cancer development and progression in hepatocellular carcinoma. However, little is known about the potential prognostic value and underlying molecular features of exosome-related long non-coding RNAs. METHODS: Genes associated with exosome biogenesis, exosome secretion, and exosome biomarkers were collected. Exosome-related lncRNA modules were identified using PCA and WGCNA analysis. A prognostic model based on data from the TCGA, GEO, NODE, and ArrayExpress was developed and validated. A comprehensive analysis of the genomic landscape, functional annotation, immune profile, and therapeutic responses underlying the prognostic signature was performed on multi-omics data, and bioinformatics methods were also applied to predict potential drugs for patients with high risk scores. qRT-PCR was used to validate the differentially expressed lncRNAs in normal and cancer cell lines. RESULTS: Twenty-six hub lncRNAs were identified as highly correlated with exosomes and overall survival and were used for prognosis modeling. Three cohorts consistently showed higher scores in the high-risk group, with an AUC greater than 0.7 over time. These higher scores implied poorer overall survival, higher genomic instability, higher tumor purity, higher tumor stemness, pro-tumor pathway activation, lower anti-tumor immune cell and tertiary lymphoid structure infiltration, and poor responses to immune checkpoint blockade therapy and transarterial chemoembolization therapy. CONCLUSION: Through developing an exosome-related lncRNA predictor for HCC patients, we revealed the clinical relevance of exosome-related lncRNAs and their potential as prognostic biomarkers and therapeutic response predictors.