Fluorescence and photoacoustic (FL/PA) dual-modal probe: Responsive to reactive oxygen species (ROS) for atherosclerotic plaque imaging.

Accurate and early detection of atherosclerosis (AS) is imperative for their effective treatment. However, fluorescence probes for efficient diagnosis of AS often encounter insufficient deep tissue penetration, which hinders the reliable assessment of plaque vulnerability. In this work, a reactive oxygen species (ROS) activated near-infrared (NIR) fluorescence and photoacoustic (FL/PA) dual model probe TPA-QO-B is developed by conjugating two chromophores (TPA-QI and O-OH) and ROS-specific group phenylboronic acid ester. The incorporation of ROS-specific group not only induces blue shift in absorbance, but also inhibits the ICT process of TPA-QO-OH, resulting an ignorable initial FL/PA signal. ROS triggers the convertion of TPA-QO-B to TPA-QO-OH, resulting in the concurrent amplification of FL/PA signal. The exceptional selectivity of TPA-QO-B towards ROS makes it effectively distinguish AS mice from the healthy. The NIR emission can achieve a tissue penetration imaging depth of 0.3 cm. Moreover, its PA775 signal possesses the capability to penetrate tissues up to a thickness of 0.8 cm, ensuring deep in vivo imaging of AS model mice in early stage. The ROS-triggered FL/PA dual signal amplification strategy improves the accuracy and addresses the deep tissue penetration problem simultaneously, providing a promising tool for in vivo tracking biomarkers in life science and preclinical applications.

Surface-modified composites of metal-organic framework and wood-derived carbon for high-performance supercapacitors.

The renewable nature, high carbon content, and unique hierarchical structure of wood-derived carbon make it an optimal self-supporting electrode for energy storage. However, the limitations in specific surface area and electrical conductivity defects pose challenges to achieving satisfactory charge storage in wood-derived carbon electrodes. Therefore, exploring diverse and effective surface strategies is crucial for enhancing the electrochemical energy storage performance. Herein, a decoration technique for enhancing aesthetic appeal involves applying a metal-organic framework (Ni/Co-MOF) containing nickel and cobalt onto the inner walls of wood tracheids. The sequential modification steps include carbonization, oxidation activation, and acid-etching. The Ni/NiO/CoO-CW-4 electrode, made by acid-etching carbonized wood (CW) doped with nickel, nickel oxide, and cobalt oxide for 4 h, has excellent surface area and pore size distribution, high graphitization degree, and exceptional conductivity. Furthermore, surface modification optimizes the surface chemistry and phase composition, resulting in a 0.8 mm thick Ni/NiO/CoO-CW-4 electrode with an exceptionally high areal capacitance of 16.76 F cm-2 at 5 mA cm-2. Meanwhile, the fabricated solid-state supercapacitor achieves an impressive energy density of 0.67 mWh cm-2 (8.38 mWh cm-3) at 2.5 mW cm-2 (31.25 mW cm-3), surpassing representative modified wood-based carbon electrodes by approximately 2-7 times. Additionally, the supercapacitor demonstrates exceptional stability, maintaining 96.21 % of capacitance even over 10,000 cycles. The parameters presented here demonstrate a significant improvement compared to those typically observed in most modified wood-derived carbon-based supercapacitors, effectively addressing common issues of low energy density and suboptimal cycling performance with wood carbon composites.

Tumour cell-released autophagosomes promote lung metastasis by upregulating PD-L1 expression in pulmonary vascular endothelial cells in breast cancer.

PURPOSE: Establishing an immunosuppressive premetastatic niche (PMN) in distant organs is crucial for breast cancer metastasis. Vascular endothelial cells (VECs) act as barriers to transendothelial cell migration. However, the immune functions of PMNs remain unclear. Tumour cell-released autophagosomes (TRAPs) are critical modulators of antitumour immune responses. Herein, we investigated the mechanism through which TRAPs modulate the immune function of pulmonary VECs in lung PMN in breast cancer. METHODS: Immortalised mouse pulmonary microvascular endothelial cells were incubated with TRAPs in vitro. RNA sequencing, flow cytometry, and western blotting were employed to assess immunosuppressive function and mechanism. In vivo, TRAP-trained and autophagy-deficient tumour mice were used to detect immunosuppression, and high-mobility group box 1 (HMGB1)-deficient TRAP-trained and TLR4 knockout mice were utilised to investigate the underlying mechanisms of pulmonary VECs. Additionally, the efficacy of anti-programmed cell death ligand-1 (PD-L1) immunotherapy was evaluated in early tumour-bearing mice. RESULTS: HMGB1 on TRAPs surfaces stimulated VECs to upregulate PD-L1 via a TLR4-MyD88-p38/STAT3 signalling cascade that depended on the cytoskeletal movement of VECs. Importantly, PD-L1 on TRAP-induced VECs can inhibit T cell function, promote lung PMN immunosuppression, and result in more pronounced lung metastasis. Treatment with anti-PD-L1 reduces lung metastasis in early stage tumour-bearing mice. CONCLUSIONS: These findings revealed a novel role and mechanism of TRAP-induced immunosuppression of pulmonary VECs in lung PMN. TRAPs and their surface HMGB1 are important therapeutic targets for reversing immunosuppression, providing a new theoretical basis for the treatment of early stage breast cancer using an anti-PD-L1 antibody.

Fibroblast growth factor 1 (FGF1) improves glucose homeostasis, modulates gut microbial composition, and reduces inflammatory responses in rainbow trout (Oncorhynchus mykiss) fed a high-fat diet.

High-fat diets (HFDs) are widely used in aquaculture due to their lipid and protein-conserving effects, thereby reducing feed costs. However, prolonged feeding of HFD often leads to metabolic disorders in fish, such as disruption of hepatic lipid homeostasis, liver injury, and disruption of glucose homeostasis. Fibroblast growth factor 1 (FGF1) plays an essential role in controlling glucose levels in the body and dampening immune reactions. However, its impact on teleosts remains poorly researched. The therapeutic potential of recombinant FGF1 (rFGF1) was examined in a 6-week culture experiment involving rainbow trout (Oncorhynchus mykiss) that were fed an HFD. The results revealed that rFGF1 significantly reduced serum glucose levels and hepatic PEPCK and G6PC activities, but improved hepatic glycogen (P < 0.05), compared to the HFD + PBS group. Further experiments indicated that the inhibitory effect of rFGF1 on hepatic gluconeogenesis was mediated by the cAMP signaling pathway and was dependent on the high expression of PDE4D. In addition, rFGF1 increased hepatic glycogen content, which involves the AKT-GSK3ß axis. Despite this increase, rFGF1 did not lead to glycogen storage disease, as shown by reduced hepatic inflammation as a result of decreased GOT (glutamic oxaloacetic transaminase), GPT (glutamic pyruvic transaminase), and elevated SOD (superoxide dismutase) in the rFGF1-treated group, accompanied by decreased il-1ß, il-6, and xbp-1, and elevated nrf2 and number of hepatocyte autophagosomes. Alterations in gut microbes and short-chain fatty acids (SCFAs) were noted, indicating that rFGF1 caused a notable rise in intestinal Lactobacillus, acetic acid, and butyric acid levels. This study investigated the molecular mechanisms of rFGF1 on glucose metabolism and inflammatory responses in an HFD-fed rainbow trout model, providing new insights to improve the regulation of glucose metabolism in carnivorous fish.

Role of macrophages in aortic dissection pathogenesis: insights from preclinical studies to translational prospective.

Aortic dissection is a critical vascular disease that is characterized by a high mortality rate and inflammation significantly influences its onset and progression. Recent studies highlight the integral role of macrophages, key players in the immune system, in the pathological landscape of aortic dissection. These cells are involved in crucial processes, such as the remodeling of the extracellular matrix, immunocyte infiltration, and phenotypic switching of smooth muscle cells, which are essential for the structural integrity and functional dynamics of the aortic wall. Despite these insights, the specific contributions of macrophages to the development and progression of aortic dissection remains unclear. This review explores the pathogenesis of aortic dissection with a focus on macrophages and describes their origins, phenotypic variations, and potential roles based on the most recent research findings. Furthermore, we discuss key molecules related to macrophages during aortic dissection, their interactions with other cellular components within the aorta, and the implications of these interactions for future therapeutic strategies. This comprehensive analysis aimed to improve our understanding of macrophages in aortic dissection and promote the development of targeted interventions.

Non-dietary exposure to phthalates in primary school children: Risk and correlation with anthropometric indices, cardiovascular and respiratory diseases.

Phthalates are endocrine disruptors of increasing concern for human health; however, previous studies have only assessed the association between internal exposure and human health. We aimed to assess the non-carcinogenic and carcinogenic risks of non-dietary exposure to phthalates in indoor environments among primary school children and their correlations with health indicators. A study involving 54 children was conducted in Jinan, Shandong Province, China. Questionnaires and health examinations were conducted, dust in hard-to-clean corners of students' classrooms and homes was collected, and airborne phthalates in the middle of classrooms and family living rooms were sampled. The gas-phase phthalate concentrations, individual exposure, and non-carcinogenic and carcinogenic risks were calculated. Associations were estimated using linear mixed models. The findings revealed that phthalates posed a non-carcinogenic risk to 7.4 % of the children and a moderate carcinogenic risk to 27.8 % of the children, with higher non-carcinogenic and carcinogenic risks to girls than to boys. Five phthalates were negatively correlated with body mass index, dimethyl phthalate and diethyl phthalate (DEP) were significantly correlated with waist circumference, and di-iso-butyl phthalate (DiBP) was negatively correlated with hip circumference. DiBP, di-n-butyl phthalate, and DEP, were significantly correlated with cardiovascular disease, DEP and di (2-n-butoxyethyl) phthalate were correlated with decreased lung function, and di-n-octyl phthalate influenced airway inflammation. The findings indicated that phthalate exposure may negatively impact children's health, thereby warranting further comprehensive research on the health effects of these chemicals.

N-Acetylcysteine Inhibits Coxsackievirus B3 Replication by Downregulating Eukaryotic Translation Elongation Factor 1 Alpha 1.

Group B Coxsackieviruses (CVB) are one of the causative pathogens of myocarditis, which may progress to cardiomyopathy. The pathogenesis of CVB is not fully understood, and effective antiviral therapy is not available. N-acetylcysteine (NAC), the classic antioxidant, has been used in clinical practice for several decades to treat various medical conditions. In this study, the anti-CVB effect of NAC was investigated. We show that NAC dramatically suppressed viral replication and alleviated cardiac injury induced by CVB3. To further study the antiviral mechanism of NAC, RNA-sequencing was performed for CVB3-infected cells with NAC treatment. We found that eukaryotic elongation factor 1 alpha 1 (EEF1A1) is one of the most upregulated genes in CVB3-infected cells. However, EEF1A2, the highly homologous isoform of EEF1A1, remains unchanged. EEF1A1 expression was significantly suppressed by NAC treatment in CVB3-infected cells, while EEF1A2 was not affected. eEF1A1 knockdown significantly inhibited CVB3 replication, implicating that eEF1A1 facilitates viral replication. Importantly, we show that eEF1A1, which was not expressed in the myocardia of newborn mice, was significantly upregulated by CVB3 infection. NAC markedly downregulated the expression of eEF1A1 but not eEF1A2 in the myocardia of CVB3-infected mice. Furthermore, NAC accelerated eEF1A1 degradation by promoting autophagy in CVB3-infected cells. We show that p62, one of the critical adaptors of autophagic targets, interacts with eEF1A1 and was downregulated in CVB3-infected cells upon NAC treatment. Taken together, this study demonstrated that NAC shows a potent anti-CVB effect through the downregulation of eEF1A1.

Proteome-wide copy-number estimation from transcriptomics.

Protein copy numbers constrain systems-level properties of regulatory networks, but proportional proteomic data remain scarce compared to RNA-seq. We related mRNA to protein statistically using best-available data from quantitative proteomics and transcriptomics for 4366 genes in 369 cell lines. The approach starts with a protein's median copy number and hierarchically appends mRNA-protein and mRNA-mRNA dependencies to define an optimal gene-specific model linking mRNAs to protein. For dozens of cell lines and primary samples, these protein inferences from mRNA outmatch stringent null models, a count-based protein-abundance repository, empirical mRNA-to-protein ratios, and a proteogenomic DREAM challenge winner. The optimal mRNA-to-protein relationships capture biological processes along with hundreds of known protein-protein complexes, suggesting mechanistic relationships. We use the method to identify a viral-receptor abundance threshold for coxsackievirus B3 susceptibility from 1489 systems-biology infection models parameterized by protein inference. When applied to 796 RNA-seq profiles of breast cancer, inferred copy-number estimates collectively re-classify 26-29% of luminal tumors. By adopting a gene-centered perspective of mRNA-protein covariation across different biological contexts, we achieve accuracies comparable to the technical reproducibility of contemporary proteomics.

Galectin-9 activates host immune response and improve immunoprotection of Onychostoma macrolepis against Aeromonas hydrophila infection.

Galectin-9 (Gal-9) belongs to a family of the glycan-binding proteins (GBPs) and is known to restrict bacterial activity via interacting with pathogen associated molecular pattern (PAMPs). However, the underlying immune mechanism of endogenous Gal-9 on fish against bacterial infection is still unclear. In this study, effects of Gal-9 from Onychostoma macrolepis (OmGal-9) on expression of immune-related genes were measured by HEK293T. The immune response of O. macrolepis with OmGal-9 overexpression to Aeromonas hydrophila (A. hydrophila) infection (1.65 × 108 CFU/mL) was evaluated by tissue bacterial load, fish survival rate and transcriptome analysis. The results showed that OmGal-9 displayed a punctate distribution in the nucleus and cytoplasm of HEK293T cells. Compared to cells transfected with the empty vector (EV group), recombinant plasmid pEGFP-Gal9 treatment (Gal9 group) significantly down-regulated the expression of immune-related genes TNFα, STAT3, MyD88, LCK, and p52 of HEK293T cells stimulated with LPS at 24 h, while up-regulated IκBα and caspase-1 (P < 0.05). The activities of catalase (CAT), superoxide dismutase (SOD), the total antioxidant capacity (T-AOC), alkaline phosphatase (AKP), acid phosphatase (ACP), and lysozyme (LZM) of O. macrolepis were significantly increased on 7 days in Gal9 group compared to EV group (P < 0.05). The bacterial load of liver, spleen, and kidney of O. macrolepis infected with A. hydrophila in Gal9 group at 24 h was significantly lower than that in EV group (P < 0.05), and the survival rate had increased from 15 % to 35 %. A comparative transcriptome analysis between the Gal9 and EV group identified 305 differentially expressed genes (DEGs). The analysis showed that OmGal-9 might play an important regulatory role in glycolysis/gluconeogenesis, fatty acid degradation, and ascorbate and aldarate metabolism. Moreover, the immune-related DEGs were predominantly enriched in eleven pathways, with the most important three of them being linked to innate immunity: NOD-like, C-type lectin and Toll-like receptor signaling pathway. Taking together, OmGal-9 can enhance the resistance of fish to bacterial diseases by improving immune system function and activating immune-related pathways.

The underlying molecular mechanisms of hormonal regulation of fruit color in fruit-bearing plants.

Fruit color is a key feature of fruit quality, primarily influenced by anthocyanin or carotenoid accumulation or chlorophyll degradation. Adapting the pigment content is crucial to improve the fruit's nutritional and commercial value. Genetic factors along with other environmental components (i.e., light, temperature, nutrition, etc.) regulate fruit coloration. The fruit coloration process is influenced by plant hormones, which also play a vital role in various physiological and biochemical metabolic processes. Additionally, phytohormones play a role in the regulation of a highly conserved transcription factor complex, called MBW (MYB-bHLH-WD40). The MBW complex, which consists of myeloblastosis (MYB), basic helix-loop-helix (bHLH), and WD40 repeat (WDR) proteins, coordinates the expression of downstream structural genes associated with anthocyanin formation. In fruit production, the application of plant hormones may be important for promoting coloration. However, concerns such as improper concentration or application time must be addressed. This article explores the molecular processes underlying pigment formation and how they are influenced by various plant hormones. The ABA, jasmonate, and brassinosteroid increase anthocyanin and carotenoid formation, but ethylene, auxin, cytokinin, and gibberellin have positive as well as negative effects on anthocyanin formation. This article establishes the necessary groundwork for future studies into the molecular mechanisms of plant hormones regulating fruit color, ultimately aiding in their effective and scientific application towards fruit coloration.

Unveiling cold Code: Acinetobacter calcoaceticus TY1's adaptation strategies and applications in nitrogen treatment.

Overcoming low nitrogen removal efficiency at low temperatures is a challenge in biological treatment. This study investigated the cold-tolerant heterotrophic nitrification-aerobic denitrification by Acinetobacter calcoaceticus TY1. Transcriptomic and biochemical analyses indicated that strain TY1 upregulated genes for energy production, assimilation, cell motility, and antioxidant enzyme production under cold stress, maintaining functions such as energy supply, nitrogen utilization, and oxidative defense. Increasing the synthesis of extracellular polysaccharides, unsaturated fatty acids, and medium-chain fatty acids and secreting large amounts of antioxidant enzymes ensured cell membrane flexibility while enhancing the antioxidant system. Immobilization experiments showed that biofilms accelerated the removal of nitrogen pollutants and demonstrated good stability, with carriers being reusable to five times, maintaining high ammonia nitrogen (63.90 %) and total nitrogen (50.66 %) removal rates. These findings reveal the cold tolerance mechanisms of strain TY1 and its excellent practical potential as a candidate for wastewater treatment in cold regions.

Single-cell RNA sequencing reveals microenvironmental infiltration in non-small cell lung cancer with different responses to immunotherapy.

BACKGROUND: Immunotherapy represents a groundbreaking and monumental achievement in the field of cancer therapy, marking a significant advancement in fighting against this devastating disease. Lung cancer has showed consistent clinical improvements in response to immunotherapy treatments, yet, it is undeniable that challenges such as limited response rates acquire resistance, and the unclear fundamental mechanisms were inevitable problems. METHODS: The cellular composition was defined and distinguished through single-cell RNA sequencing (scRNA-seq) analysis of MPR (major pathologic response) and NMPR (non-major pathologic response) samples in GSE207422, including four primary MPR samples and eight primary NMPR samples. RESULTS: We found obvious difference in CD8+ T cell population between MPR and NMPR samples, with high expression of TYMS, RRM2, and BIRC5 in NPMR samples. Meanwhile, the proportion of macrophages and tumor epithelial cells infiltration increased in the NMPR samples. We discovered biomarkers (ACTN4, ATF3, BRD2, CDKN1A, and CHMP4B) in epithelial cells which were potentially represented worse outcomes. CONCLUSIONS: By exploring the difference of tumor microenvironment (TME) in samples with different corresponding degrees of neoadjuvant immunotherapy, this research introduces a number of novel biomarkers for predicting the response of treatment and a theoretical basis for overcoming immunotherapy resistance.

A Wide-Bandwidth Inexpensive Current Sensor Based on the Signal Fusion of Tunneling Magnetoresistance and a Current Transformer.

In technology and industrial production, many applications require wide-bandwidth current measurements. In this paper, a signal fusion scheme for a current sensor comprising tunneling magnetoresistance and a current transformer is proposed, achieving a flat frequency response in the DC to MHz range. The measurement principles in different cases of the scheme are introduced, and the total transfer function of the entire scheme is derived by analyzing each section separately. Furthermore, the feasibility and selected parameters of the scheme are verified through a systematic simulation utilizing the MATLAB software. Based on the proposed scheme, a group of principal prototypes are built to experimentally evaluate the bandwidth, amplitude and phase flatness, accuracy, sensitivity, and impulse response. The relative amplitude variation in the passband of the fusion sensor is less than 4%, and the estimated bandwidth of the fusion sensor is close to 17 MHz. The accuracy is better than 0.6%, even when measuring the current at 1 MHz, and the relative standard deviation is 5% when measuring the impulse signal. The sensors developed using this scheme, with a low financial cost, have advantages in many wide-bandwidth current measuring scenarios.

Endovascular Perclose ProGlide complication puncture site, treated successful by cutting balloon dilatation: A case report and literature review.

Perclose ProGlide were created as preferred for puncture site closure of femoral artery. Femoral artery occlusion is one of the serious device-related complications. This report presents a continuous endovascular technique combined with peripheral cutting balloon (PCB) treatment for a case of a 32s woman diagnosed with lower extremity ischaemia caused by right superficial femoral artery (SFA) occlusion following the use of the Perclose ProGlide system in minimally invasive cardiac surgery. During the primary operation, limb ischaemia symptoms were relieved with vessel perfusion and reconstruction after regular balloon dilatation. A secondary operation was conducted 6 weeks later, and the obstructive lesions were recanalised without residual stenosis after PCB dilatation. No vessel-related adverse events such as dissection, rupture or distal embolisation occurred during the perioperative period. The patient recovered uneventfully after the operation, with complete alleviation of symptoms. Follow-up computed tomography angiography 3 month post-operatively revealed an undeformed shape and excellent patency of the right SFA.

In Situ Heparan Sulfate-Induced Peptide Self-Assembly to Overcome the Cell Surface Glycocalyx Barrier for Cancer Treatment.

Heparan sulfate (HS) is a major component of cell surface glycocalyx with extensive negative charges and plays a protective role by preventing toxins, including small molecule drugs and anticancer cationic lytic peptides (ACLPs), from cells. However, this effect may compromise the treatment efficiency of anticancer drugs. To overcome the impedance of cancer cell glycocalyx, an HS-targeting ACLP PTP-7z was designed by fusion of an ACLP and a Zn2+-binding HS-targeting peptide. Upon Zn2+ ion binding, PTP-7z could self-assemble into uniform nanoparticles and show improved serum stability and reduced hemolysis, which enable it to self-deliver to tumor sites. The peptide PTP-7z showed a pH- and Zn2+ ion-dependent HS-binding ability, which triggers the HS-induced in situ self-assembling on the cancer cell surface in the acidic tumor microenvironment (TME). The self-assembled PTP-7z can overcome the impedance of cell glycocalyx by either disrupting cell membranes or translocating into cells through endocytosis and inducing cell apoptosis. Moreover, PTP-7z can also inhibit cancer cell migration. These results proved that HS-responsive in situ self-assembling is a practical strategy to overcome the cancer cell glycocalyx barrier for ACLPs and could be extended to the design of other peptide drugs to promote their in vivo application.

Bispecific CAR-T cells targeting CD19/20 in patients with relapsed or refractory B cell non-Hodgkin lymphoma: a phase I/II trial.

Non-Hodgkin lymphoma (NHL) is a common malignancy in the hematologic system, and traditional therapy has limited efficacy for people with recurrent/refractory NHL (R/R NHL), especially for patients with diffuse large B cell lymphoma (DLBCL). Chimeric antigen receptor (CAR) T-cell therapy is a novel and effective immunotherapy strategy for R/R hematopoietic malignancies, but relapses can occur due to the loss of CAR-T cells in vivo or the loss of antigen. One strategy to avoid antigen loss after CAR-T cell therapy is to target one more antigen simultaneously. Tandem CAR targeting CD19 and CD22 has demonstrated the reliability of tandem CAR-T cell therapy for R/R B-ALL. This study explores the therapeutic potential of tandem CD19/20 CAR-T in the treatment of R/R B cell NHL. The efficacy and safety of autologous CD19/20 CAR-T cells in eleven R/R B cell NHL adult patients were evaluated in an open-label, single-arm trial. Most patients achieved complete response, exhibiting the efficacy and safety of tandem CD19/20 CAR-T cells. The TCR repertoire diversity of CAR-T cells decreased after infusion. The expanded TCR clones in vivo were mainly derived from TCR clones that had increased expression of genes associated with immune-related signaling pathways from the infusion product (IP). The kinetics of CAR-T cells in vivo were linked to an increase in the expression of genes related to immune response and cytolysis/cytotoxicity.

BioLadder: A bioinformatic platform primarily focused on proteomic data analysis.

BioLadder (https://www.bioladder.cn/) is an online data analysis platform designed for proteomics research, which includes three classes of experimental data analysis modules and four classes of common data analysis modules. It allows for a variety of proteomics analyses to be conducted easily and efficiently. Additionally, most modules can also be utilized for the analysis of other omics data. To facilitate user experience, we have carefully designed four different kinds of functions for customers to quickly and accurately utilize the relevant analysis modules.

mRNA expression insights: Unraveling the relationship between COPD and lung cancer.

BACKGROUND: Lung cancer is a prevalent form of cancer worldwide. A possible link between lung cancer and chronic obstructive pulmonary disease (COPD) has been suggested by recent studies. The objective of our research was to analyze the mRNA expression patterns in both situations, with a specific emphasis on their biological functions and the pathways they are linked to. METHOD: Data on COPD mRNA expression was collected from the NCBI-GEO database, while information regarding lung cancer mRNA was acquired from The Cancer Genome Atlas database. To examine the association of COPD-related scores in lung cancer patients, we utilized the ssGSEA algorithm for single sample gene set enrichment analysis. The possible routes were examined through the utilization of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Risk models were developed using Cox and least absolute shrinkage and selection operator (LASSO) regression analyses. Moreover, a GSEA was performed to investigate significant pathways among various risk groups. RESULT: After identifying 17 genes that were differentially expressed and linked to COPD, we found that they met the criteria of having a false discovery rate < 0.05 and an absolute log2 fold change > 0.585. By utilizing the ssGSEA algorithm, it became possible to classify individuals with lung cancer into two distinct groups based on their COPD status. Consequently, a seven-gene risk model was developed specifically for these patients. The risk score was determined by applying the given formula: risk score = AC022784.1 × 0.0423737993775888 + CRISP3 × 0.0415322046890524 + MELTF × 0.0661848418476596 + MT2P1 × 0.111843227536117 + FAM83A-AS1 × 0.045295939710361 + ZNF506 × -0.309489953363417 + ITGA6 × 0.01813978449589. The risk model associated with COPD showed a notable connection with different immune cells found in the lung cancer sample, including macrophages of M0/M1/M2 types, hematopoietic stem cells, mast cells, NK T cells and regulatory T cells. Overexpression of crucial genes was seen to enhance cell proliferation and invasive potential in the lung cancer sample. In the lung cancer sample, it was observed that an increase in ZNF506 expression enhanced both cell proliferation and invasion. CONCLUSION: In conclusion, this study effectively examines the potential correlation between COPD and lung cancer. A prognostic model based on seven COPD-associated genes demonstrated robust predictive potential in the lung cancer sample. Our analysis offers comprehensive insights for lung cancer patients.