Chemokines and Their Receptors: Predictors of Therapeutic Potential in Tumor Microenvironment on Esophageal Cancer.

Esophageal carcinoma (ESCA) is an aggressive solid tumor. The 5-year survival rate for patients with ESCA is estimated to be less than 20%, mainly due to tumor invasion and metastasis. Therefore, it is urgent to improve early diagnostic tools and effective treatments for ESCA patients. Tumor microenvironment (TME) enhances the ability of tumor cells to proliferate, migrate, and escape from the immune system, thus promoting the occurrence and development of tumor. TME contains chemokines. Chemokines consist of four major families, which are mainly composed of CC and CXC families. The main purpose of this review is to understand the CC and CXC chemokines and their receptors in ESCA, to improve the understanding of tumorigenesis of ESCA and determine new biomarkers for the diagnosis and prognosis of ESCA. We reviewed the literature on CC and CXC chemokines and their receptors in ESCA identified by PubMed database. This article introduces the general structures and functions of CC, CXC chemokines and their receptors in TME, as well as their roles in the progress of ESCA. Chemokines are involved in the development of ESCA, such as cancer cell invasion, metastasis, angiogenesis, and radioresistance, and are key determinants of disease progression, which have a great impact on patient prognosis and treatment response. In addition, a full understanding of their mechanism of action is essential to further verify that these chemokines and their receptors may serve as biomarkers or therapeutic targets of ESCA.

Identification of qualitative characteristics of immunosuppression in sepsis based on immune-related genes and immune infiltration features.

Objective: Sepsis is linked to high morbidity and mortality rates. Consequently, early diagnosis is crucial for proper treatment, reducing hospitalization, and mortality rates. Additionally, over one-fifth of sepsis patients still face a risk of death. Hence, early diagnosis, and effective treatment play pivotal roles in enhancing the prognosis of patients with sepsis. Method: The study analyzed whole blood data obtained from patients with sepsis and control samples sourced from three datasets (GSE57065, GSE69528, and GSE28750). Commonly dysregulated immune-related genes (IRGs) among these three datasets were identified. The differential characteristics of these common IRGs in the sepsis and control samples were assessed using the REO-based algorithm. Based on these differential characteristics, samples from eight Gene Expression Omnibus (GEO) databases (GSE57065, GSE69528, GSE28750, GSE65682, GSE69063, GSE95233, GSE131761, and GSE154918), along with three ArrayExpress databases (E-MTAB-4421, E-MTAB-4451, and E-MTAB-7581), were categorized and scored. The effectiveness of these differential characteristics in distinguishing sepsis samples from control samples was evaluated using the AUC value derived from the receiver operating characteristic curve (ROC) curve. Furthermore, the expression of IRGs was validated in peripheral blood samples obtained from patients with sepsis through qRT-PCR. Results: Among the three training datasets, a total of 84 common dysregulated immune-related genes (IRGs) were identified. Utilizing a within-sample relative expression ordering (REOs)-based algorithm to analyze these common IRGs, differential characteristics were observed in three reverse stable pairs (ELANE-RORA, IL18RAP-CD247, and IL1R1-CD28). In the eight GEO datasets, the expression of ELANE, IL18RAP, and IL1R1 demonstrated significant upregulation, while RORA, CD247, and CD28 expression exhibited notable downregulation during sepsis. These three pairs of immune-related marker genes displayed accuracies of 95.89% and 97.99% in distinguishing sepsis samples among the eight GEO datasets and the three independent ArrayExpress datasets, respectively. The area under the receiver operating characteristic curve ranged from 0.81 to 1.0. Additionally, among these three immune-related marker gene pairs, mRNA expression levels of ELANE and IL1R1 were upregulated, whereas the levels of CD247 and CD28 mRNA were downregulated in blood samples from patients with sepsis compared to normal controls. Conclusion: These three immune-related marker gene pairs exhibit high predictive performance for blood samples from patients with sepsis. They hold potential as valuable auxiliary clinical blood screening tools for sepsis.

Swarm intelligence based deep learning model via improved whale optimization algorithm and Bi-directional long short-term memory for fault diagnosis of chemical processes.

The chemical production process typically possesses complexity and high risks. Effective fault diagnosis is a key technology for ensuring the reliability and safety of chemical production processes. In this study, a comprehensive fault diagnosis method based on time-varying filtering empirical mode decomposition (TVF-EMD), kernel principal component analysis (KPCA), and an improved whale optimization algorithm (WOA) to optimize bi-directional long short-term memory (BiLSTM) is proposed. This research utilizes TVF-EMD and KPCA to analyze and preprocess the raw data, eliminating noise and and reducing the dimensions of the fault data. Subsequently, BiLSTM is employed for fault data classification. To address the hyperparameters within BiLSTM, the enhanced WOA is used for optimization. Finally, the efficacy and superiority of this approach are validated through two fault diagnosis examples.

Histomorphological analysis of perfusion parameters and CNS lymphatic vessels in mice: an experimental method study.

To investigate the distribution and characteristics of lymphatic vessels within the central nervous system, we focus on the meninges of the spinal cord and brain parenchyma in mice. Additionally, we aim to provide experimental methods for obtaining optimal imaging and clear structures of lymphatic vessels, while optimizing the perfusion parameters to improve histomorphological quality. Male C57BL/6J mice were randomly divided into four groups, with each group assigned a specific perfusion parameter based on perfusion volumes and temperatures. Immunofluorescence staining of lymphatics and blood vessels was performed on both meningeal and the brain tissue samples. Statistical analysis was performed using one-way analysis of variance to compare the groups, and a significant level of P < 0.05 was considered statistically significant. Our study reports the presence of lymphatic vessels in the meninges of the spinal cord and brain parenchyma in mice. We highlight the crucial role of high perfusion volume of paraformaldehyde with low temperature in fixation for achieving optimal results. We provide experimental methods for obtaining optimal imaging and clear structures of lymphatic vessels in the meninges of the spinal cord and brain parenchyma in mice, which contribute to our understanding of the distribution and characteristics of lymphatic vessels within the central nervous system. Further research is warranted to explore the functional implications of these lymphatic vessels and their potential therapeutic significance in neurodegenerative and neuroinflammatory diseases.

Inhibition of CISD1 alleviates mitochondrial dysfunction and ferroptosis in mice with acute lung injury.

The NET family member, CDGSH iron-sulfur domain-containing protein 1 (CISD1), is located in theoutermembrane of mitochondria, where it regulates energy and iron metabolism. CISD1 has vital functions in certain human diseases; however, its function in acute lung injury (ALI) is unknown. ALI pathogenesis critically involves mitochondrial dysfunction and ferroptosis, which might be regulated by CISD1. Therefore, we investigated CISD1's function in mitochondrial dysfunction and ferroptosis regulation in lipopolysaccharide (LPS)-induced ALI. We found that CISD1 was upregulated in LPS-induced ALI,and silencing Cisd1 prevented cell apoptosis and increased cell viability. When CISD1was inhibited by mitoNEET ligand-1 (NL-1) there was a significant mitigation of pathological injury and lung edema, and reduced numbers of total cells, polymorphonuclear leukocytes, and a decreased protein content in the bronchoalveolar lavage fluid (BALF). Moreover, inhibition of CISD1 markedly decreased the interleukin (IL)6, IL-1ß, and tumor necrosis factor alpha (TNF-α) levels in the lungs and BALF of ALI-model mice. Silencing of Cisd1 prevented LPS-induced mitochondrial membrane potential depolarization, cellular ATP reduction, and reactive oxygen species (ROS) accumulation, suggesting mitochondrial protection. ALI activated ferroptosis, as evidenced by the increased lipid-ROS, intracellular Fe2+ level, reduced Gpx4 (glutathione peroxidase 4) expression, and the glutathione/glutathione disulfide ratio. Interestingly, inhibition of CISD1 reduced LPS-induced ferroptosis in vivo and in vitro. In conclusion, inhibition of CISD1 alleviated mitochondrial dysfunction and ferroptosis in LPS-induced ALI, identifying CISD1 as possible target for therapy of LPS-induced ALI.

Skeleton-Based Activity Recognition for Process-Based Quality Control of Concealed Work via Spatial-Temporal Graph Convolutional Networks.

Computer vision (CV)-based recognition approaches have accelerated the automation of safety and progress monitoring on construction sites. However, limited studies have explored its application in process-based quality control of construction works, especially for concealed work. In this study, a framework is developed to facilitate process-based quality control utilizing Spatial-Temporal Graph Convolutional Networks (ST-GCNs). To test this model experimentally, we used an on-site collected plastering work video dataset to recognize construction activities. An ST-GCN model was constructed to identify the four primary activities in plastering works, which attained 99.48% accuracy on the validation set. Then, the ST-GCN model was employed to recognize the activities of three extra videos, which represented a process with four activities in the correct order, a process without the activity of fiberglass mesh covering, and a process with four activities but in the wrong order, respectively. The results indicated that activity order could be clearly withdrawn from the activity recognition result of the model. Hence, it was convenient to judge whether key activities were missing or in the wrong order. This study has identified a promising framework that has the potential to the development of active, real-time, process-based quality control at construction sites.

Golden bifid treatment regulates gut microbiota and serum metabolites to improve myocardial dysfunction in cecal ligation and puncture-induced sepsis mice.

Myocardial damage is a major consequence and a significant contributor to death in cases of sepsis, a severe infection characterized by a distinct inflammatory response and a potential threat to the patient's life. Recently, the effects of intestinal microbiota and serum metabolites on sepsis have garnered increasing attention. Herein, the effects of golden bifid treatment upon cecal ligation and puncture (CLP)-induced sepsis in mice as a model for myocardial dysfunction were explored. Our results demonstrated that golden bifid treatment partially improved myocardial dysfunction and apoptosis, cardiac inflammation and oxidative stress, and intestinal mucosal permeability and barrier dysfunction in CLP-induced sepsis mice. The intestinal microbiota diversity and abundance were also altered within sepsis mice and improved by golden bifid treatment. Mucispirillum schaedleri, Acinetobacter baumannii and Lactobacullus intestinalis were significantly correlated with heart damage markers, inflammatory factors, or oxidative stress indicators. Serum differential metabolite levels were also significantly correlated with these parameters. Altogether, golden bifid treatment might be an underlying approach for treating sepsis-induced myocardial dysfunction and highlight the underlying effect of intestinal microbiota and serum metabolites on the pathogenesis and treatment of sepsis-triggered myocardial dysfunction.

Research and application of a novel selective stacking ensemble model based on error compensation and parameter optimization for AQI prediction.

With the ongoing process of industrialization, the issue of declining air quality is increasingly becoming a critical concern. Accurate prediction of the Air Quality Index (AQI), considered as an all-inclusive measure representing the extent of pollutants present in the atmosphere, is of paramount importance. This study introduces a novel methodology that combines stacking ensemble and error correction to improve AQI prediction. Additionally, the reptile search algorithm (RSA) is employed for optimizing model parameters. In this study, four distinct regional AQI data containing a collection of 34864 data samples are collected. Initially, we perform cross-validation on ten commonly used single models to obtain prediction results. Then, based on evaluation indices, five models are selected for ensemble. The results of the study show that the model proposed in this paper achieves an improvement of around 10% in terms of accuracy when compared to the conventional model. Thus, the model introduced in this study offers a more scientifically grounded approach in tackling air pollution.

miR-133b Promotes Esophageal Squamous Cell Carcinoma Metastasis.

Background: Evaluation of biological changes at the molecular level has important clinical implications for improving the survival rate of esophageal squamous cell carcinoma (ESCC). Therefore, we plan to analyze and elucidate the expression of microRNA-133b (miR-133b), M2 pyruvate kinase (PKM2), and signal transducer and activator of transcription 3 (STAT3) in ESCC and their associated clinicopathological significance. Methods: The 72 patients with ESCC were selected as the experimental study group. Normal adjacent tissues (NAT) were matched as the control group. In this study, in situ hybridization was used to detect the expression of miR-133b in ESCC, and tissue expressions of PKM2 and STAT3 were detected by immunohistochemistry, and literature review was conducted. Results: Studies had shown that the positive expression of miR-133b in NAT was significantly higher than that in ESCC (χ2 = 9.007, P = .003). PKM2 and STAT3 in ESCC had a significantly higher positive expression levels than those of NAT (χ2 = 56.523, P = .000; χ2 = 72.939, P = .000). From correlation analysis, there was a negative correlation between miR-133b and PKM2(r = -0.515, P < .001), a negative correlation between miR-133b and STAT3(r = -0.314, P = .007), and a positive correlation between PKM2 and STAT3(r = 0.771, P < .001). Conclusions: In ESCC, our study demonstrated that downregulation of miR-133b and upregulation of PKM2 and STAT3. We predict that miR-133b may inhibit the STAT3 pathway by downregulating PKM2.

Pyroptosis: the dawn of a new era in endometrial cancer treatment.

Endometrial cancer (EC) is a malignancy of the inner epithelial lining of the uterus. While early-stage EC is often curable through surgery, the management of advanced, recurrent and metastatic EC poses significant challenges and is associated with a poor prognosis. Pyroptosis, an emerging form of programmed cell death, is characterized by the cleavage of gasdermin proteins, inducing the formation of extensive gasdermin pores in the cell membrane and the leakage of interleukin-1ß (IL-1ß) and interleukin-18 (IL-18), consequently causing cell swelling, lysis and death. It has been found to be implicated in the occurrence and progression of almost all tumors. Recent studies have demonstrated that regulating tumor cells pyroptosis can exploit synergies function with traditional tumor treatments. This paper provides an overview of the research progress made in molecular mechanisms of pyroptosis. It then discusses the role of pyroptosis and its components in initiation and progression of endometrial cancer, emphasizing recent insights into the underlying mechanisms and highlighting unresolved questions. Furthermore, it explores the potential value of pyroptosis in the treatment of endometrial cancer, considering its current application in tumor radiotherapy, chemotherapy, targeted therapy and immunotherapy.

Inhibition of SIRT6 aggravates p53-mediated ferroptosis in acute lung injury in mice.

Although studies have shown that protein 53 (p53)-mediated ferroptosis is involved in acute lung injury (ALI), the mechanism of its regulation remains unclear. The protective effects of Sirtuin 6 (SIRT6), a histone deacetylase, have been demonstrated in multiple diseases; however, further studies are needed to elucidate the role of SIRT6 in ALI. In the present study, we hypothesize that SIRT6 protects against lipopolysaccharide (LPS)-induced ALI by regulating p53-mediated ferroptosis. We observed that the inhibition of ferroptosis prevented LPS-induced ALI. The knockout of p53 blocked LPS-induced ferroptosis and ALI, suggesting that p53 facilitated ALI by promoting ferroptosis. In addition, the inhibition of SIRT6 aggravated LPS-induced ferroptosis and ALI, while the depression of ferroptosis blocked the exacerbation of lung injury induced by SIRT6 inhibition. The results suggest that SIRT6 protects against ALI by regulating ferroptosis. Furthermore, the inhibition of SIRT6 reinforced the p53 acetylation and the deletion of p53 rescued the exacerbation of ferroptosis induced by SIRT6 inhibition. The findings indicate that SIRT6 regulates the acetylation of p53 and prevents p53-mediated ferroptosis. In conclusion, our results indicate that SIRT6 protects against LPS-induced ALI by regulating p53-mediated ferroptosis, thereby demonstrating that SIRT6 holds great promise as a therapeutic target for ALI.

Identification of ferroptotic genes and phenotypes in idiopathic nonobstructive azoospermia.

Effective treatments for nonobstructive azoospermia (NOA), which affects 1% of all men globally, are limited by undefined pathogenic mechanisms, especially in idiopathic NOA (iNOA). Here, we tried to identify the functional ferroptosis-related genes and phenotypes involved in iNOA. Differentially expressed ferroptotic genes were identified from iNOA mRNA microarray datasets by bioinformatic analyses, and these ferroptotic genes were subsequently filtered by various algorithms. Then, receiver operating characteristic (ROC) curves were generated to evaluate the diagnostic ability of the abovementioned genes for iNOA. Generally, 11 differentially expressed ferroptotic genes were downregulated, and five genes were upregulated in iNOA samples. Four genes, including DUSP1, GPX4, HSD17B11, and SLC2A8, were technically selected and determined to be potential biomarkers for iNOA. Subsequently, similar expression levels were validated at both the RNA and protein levels in the iNOA specimens. Finally, morphologic and biochemical assays were applied to define the ferroptotic phenotypes in testes. The ferroptotic features, like shrunken mitochondria with electron-dense membranes and a reduction in cristae were observed across various cell types within iNOA patients, accompanied by the overload of ferrous ions and increased lipid peroxidation production. Our findings demonstrated that these ferroptosis genes could be involved in the underlying pathogenesis mechanisms of iNOA by regulating ferroptosis and serve as potential diagnostic biomarkers. Also, the ferroptotic phenotypes were identified in iNOA patients.

Antibacterial lanostane triterpenoids from Ganoderma tsugae.

A phytochemical investigation on the 80% EtOH extract of the fruiting bodies of Ganoderma tsugae resulted into the isolation of two previously undescribed lanostane triterpenoids, 7,11-dioxo-3ß-acetyloxy-26,27-dihydroxy-lanosta-8,24-diene (1) and 7,20-dioxo-3ß-acetyloxy-11ß,15α-dihydroxy-22,23,24,25,26,27-hexanorlanosta-8-ene (2), togeher with one known lanostane triterpenoid ganodermanontriol (3). Structural elucidation of all the compounds were performed by spectral methods such as 1D and 2D (1H-1H COSY, HMQC, and HMBC) NMR spectroscopy. All the triterpenoids were in vitro evaluated for their antibacterial activities against six pathogenic microorganisms. Compound 3 exhibited some activities against three Gram positive bacteria with MIC values less than 30 µg/ml.

Association between the Triglyceride-Glucose Index and Non-Alcoholic Fatty Liver Disease in patients with Atrial Fibrillation.

BACKGROUND: The triglyceride and glucose index (TyG), as a surrogate of insulin resistance (IR), is closely associated with non-alcoholic fatty liver disease (NAFLD). However, the association between the TyG index and NAFLD in atrial fibrillation (AF) is unknown. Therefore, the purpose of this study is to explore the association between the TyG index and NAFLD in AF. METHODS: This retrospective study was performed at Nanchang University's Second Affiliated Hospital. The AF patients who were hospitalized from January 2021 to December 2022 were enrolled. The association between the TyG index and NAFLD in AF patients was assessed by logistic regression and restricted cubic spline analysis. The ability of TyG index for identifying NAFLD was estimated by the area under the receiver operating characteristic (ROC). RESULTS: In this study, 632 people participated in the final analysis, with 176 (27.84%) having NAFLD. In the full adjustment model, there is an association between the TyG index and NAFLD [per 1 unit increment; odds ratios (ORs): 3.28; 95% confidence interval (CI) 2.14, 5.03]. Compared to the lowest tertile (TyG index < 8.29), the ORs for the highest tertile (TyG index ≥ 8.82) were 4.15 (95%CI: 2.28, 7.53). Dose-response analysis showed that the TyG index and NAFLD have a nearly linear relationship (P non-linear = 0.71). The area under the curve (AUC) of the TyG index is 0.735. CONCLUSIONS: Our findings showed a significant association between the TyG index and NAFLD. The TyG index may be a good marker for predicting NAFLD in AF patients.

Advances in the detection of ß-lactamase: A review.

ß-lactamase, an enzyme secreted by bacteria, is the main resistant mechanism of Gram-negative bacteria to ß-lactam antibiotics. The resistance of bacteria to ß-lactam antibiotics can be evaluated by testing the activity of ß-lactamase. Traditional phenotypic detection is a golden principle, but it is time-consuming. In recent years, many new methods have emerged, which improve the efficiency by virtue of their sensitivity, low cost, easy operation, and other advantages. In this paper, we systematically review these researches and emphasize their limits of detection, sample operation, and test duration. Noteworthily, some detection systems can identify the ß-lactamase subtype conveniently. We mainly divide these tests into three categories to elaborate their characteristics and application status. Both advantages and disadvantages of these methods are discussed. Additionally, we analyze the recent 5 years published researches to predict the trend of development in this field.

Plant-on-chip: Core morphogenesis processes in the tiny plant Wolffia australiana.

A plant can be thought of as a colony comprising numerous growth buds, each developing to its own rhythm. Such lack of synchrony impedes efforts to describe core principles of plant morphogenesis, dissect the underlying mechanisms, and identify regulators. Here, we use the minimalist known angiosperm to overcome this challenge and provide a model system for plant morphogenesis. We present a detailed morphological description of the monocot Wolffia australiana, as well as high-quality genome information. Further, we developed the plant-on-chip culture system and demonstrate the application of advanced technologies such as single-nucleus RNA-sequencing, protein structure prediction, and gene editing. We provide proof-of-concept examples that illustrate how W. australiana can decipher the core regulatory mechanisms of plant morphogenesis.

A high-throughput drug screening identifies luteolin as a therapeutic candidate for pathological cardiac hypertrophy and heart failure.

Background: Pathological cardiac hypertrophy is commonly resulted from sustained pressure overload and/or metabolic disorder and eventually leads to heart failure, lacking specific drugs in clinic. Here, we aimed to identify promising anti-hypertrophic drug(s) for heart failure and related metabolic disorders by using a luciferase reporter-based high-throughput screening. Methods: A screen of the FDA-approved compounds based on luciferase reporter was performed, with identified luteolin as a promising anti-hypertrophic drug. We systematically examined the therapeutic efficacy of luteolin on cardiac hypertrophy and heart failure in vitro and in vivo models. Transcriptome examination was performed to probe the molecular mechanisms of luteolin. Results: Among 2,570 compounds in the library, luteolin emerged as the most robust candidate against cardiomyocyte hypertrophy. Luteolin dose-dependently blocked phenylephrine-induced cardiomyocyte hypertrophy and showed extensive cardioprotective roles in cardiomyocytes as evidenced by transcriptomics. More importantly, gastric administration of luteolin effectively ameliorated pathological cardiac hypertrophy, fibrosis, metabolic disorder, and heart failure in mice. Cross analysis of large-scale transcriptomics and drug-target interacting investigations indicated that peroxisome proliferator activated receptor γ (PPARγ) was the direct target of luteolin in the setting of pathological cardiac hypertrophy and metabolic disorders. Luteolin can directly interact with PPARγ to inhibit its ubiquitination and subsequent proteasomal degradation. Furthermore, PPARγ inhibitor and PPARγ knockdown both prevented the protective effect of luteolin against phenylephrine-induced cardiomyocyte hypertrophy in vitro. Conclusion: Our data clearly supported that luteolin is a promising therapeutic compound for pathological cardiac hypertrophy and heart failure by directly targeting ubiquitin-proteasomal degradation of PPARγ and the related metabolic homeostasis.

Early postsurgical lethal outcome due to splenic littoral cell angioma: A case report.

BACKGROUND: Littoral cell angioma (LCA) is a rare benign vascular tumor of the spleen. Given its rarity, standard diagnostic and therapeutic recommendations have yet to be developed for reported cases. Splenectomy is the only method of obtaining a pathological diagnosis and providing treatment to obtain a favorable prognosis. CASE SUMMARY: A 33-year-old female presented with abdominal pain for one month. Computed tomography and ultrasound revealed splenomegaly with multiple lesions and two accessory spleens. The patient underwent laparoscopic total splenectomy and accessory splenectomy, and splenic LCA was confirmed by pathology. Four months after surgery, the patient presented with acute liver failure, was readmitted, rapidly progressed to multiple organ dysfunction syndrome and died. CONCLUSION: Preoperative diagnosis of LCA is challenging. We systematically reviewed online databases to identify the relevant literature and found a close relationship between malignancy and immunodysregulation. When a patient suffers from both splenic tumors and malignancy or immune-related disease, LCA is possible. Due to potential malignancy, total splenectomy (including accessory spleen) and regular follow-up after surgery are recommended. If LCA is diagnosed after surgery, a comprehensive postoperative examination is needed.

Boryl Radical-Promoted Dehydroxylative Alkylation of 3-Hydroxyoxindole Derivatives.

A boryl radical-promoted dehydroxylative alkylation of 3-hydroxy-oxindole derivatives is achieved. The reaction starts from addition of 4-dimethylaminopyridine (DMAP)-boryl radical to the amide carbonyl oxygen atom, which induces a spin-center shift process to promote the C-O bond cleavage. The elimination of a hydroxide anion from a free hydroxy group is also accomplished. Capture of the generated carbon radical with alkenes furnishes a variety of C-3 alkylated oxindoles. This method features a simple operation and broad substrate scope.

Clinical application study on miR-98-5p as a prognostic biomarker in hepatocellular carcinoma.

BACKGROUND: On the one hand, to investigate the targeted regulation of miR-98-5p on heparin-binding epidermal growth factor-like growth factor (HBEGF) in patients with hepatocellular carcinoma (HCC). On the other hand, elucidate the predictive effect of miR-98-5p combined with magnetic resonance imaging (MRI) data on the clinical prognosis of HCC patients. METHODS: Serum samples from 98 HCC patients and 54 healthy subjects were selected in order to detect miR-98-5p as well as HBEGF expression levels via real-time quantitative PCR (RT-qPCR). A Luciferase reporter assay was performed to detect the interaction between miR-98-5p and HBEGF gene. The serum levels of IL-2, TNF-α, TGF-ß1 and IFN-γ in HCC patients and in the control group (healthy subjects) were measured by enzyme-linked immunosorbent assay (ELISA). In addition, receiver operator characteristic curve (ROC) was utilized to analyze the predictive ability of miR-98-5p combined with HBEGF for HCC. Finally, the survival curves were used to analyze the effect of HBEGF and miR-98-5p on the survival of patients with HCC. RESULTS: RT-qPCR results showed that the expression level of miR-98-5p was significantly decreased, while HBEGF expression was significantly increased in the serum of HCC patients compared with the control group. Luciferase reporter assay confirmed that miR-98-5p could target and bind HBEGF. Additionally, according to ELISA, IL-2, TNF-α, and TGF-ß1 were significantly increased, while IFN-γ was significantly decreased in the serum of HCC patients compared with the control group. The results of ROC indicated that expressive levels of miR-98-5p and HBEGF had a high diagnostic value for HCC. At the same time, the survival curve results indicated high HBEGF expression and low miR-98-5p expression, suggesting a poor prognosis for HCC patients. CONCLUSION: MiR-98-5p can target the down-regulating HBEGF gene. In addition, miR-98-5p combined with MRI data is of crucial guiding value in assessing the prognosis of patients with HCC in the clinic.