Novel insight into MDA-7/IL-24: A potent therapeutic target for autoimmune and inflammatory diseases.

Melanoma differentiation-associated gene-7 (MDA-7)/interleukin-24 (IL-24) is a pleiotropic member of the IL-10 family of cytokines, and is involved in multiple biological processes, including cell proliferation, cell differentiation, tissue fibrosis, the inflammatory response, and antitumor activity. MDA-7/IL-24 can regulate epithelial integrity, homeostasis, mucosal immunity and host resistance to various pathogens by enhancing immune and inflammatory responses. Our recent study revealed the mechanism of MDA-7/IL-24 in promoting airway inflammation and airway remodeling through activating the JAK/STAT3 and ERK signaling pathways in bronchial epithelial cells. Herein, we summarize the cellular sources, inducers, target cells, signaling pathways, and biological effects of MDA-7/IL-24 in several allergic and autoimmune diseases. This review also synopsizes recent advances in clinical research targeting MDA-7/IL-24 or its receptors. Based on these advancements, we emphasize its potential as a target for immunotherapy and discuss the challenges of developing immunotherapeutic drugs targeting MDA-7/IL-24 or its receptors in autoimmune and inflammatory disorders.

Clinical features of HIV positive talaromycosis marneffei patients and development of a risk prediction model.

Aims: The purpose of this study was to establish and verify a nomogram to predict the prognosis of patients with human immunodeficiency virus (HIV)-related talaromycosis marneffei and evaluate the prognosis. Methods: We examined the acquired immune deficiency syndrome (AIDS) patients hospitalized in the Fourth People's Hospital of Nanning from 2018 to 2020 with an aetiological diagnosis of Talaromyces marneffei infection. Logistic regression analysis was used to identify the independent risk factors for relapse or death of the prognosis of Talaromyces marneffei infection. According to the regression coefficient, the corresponding nomograph prediction model was drawn. Results: A total of 400 patients were included, including 321 males and 79 females. Recurrence or death occurred in 70 cases (17.5%). The area under the receiver operator characteristic curve (ROC) of the established model was 0.716 with good discrimination, calibration, and clinical effectiveness. The risks of age between 45 and 60 years old and <40 years old were successively higher than that of >60 years old, and the risks of G test <50 pg/ml and >100 pg/ml were higher than that of 50-100 pg/ml. Respiratory failure, decreased albumin and elevated total bilirubin are risk factors for relapse or death in HIV patients infected with Talaromyces marneffei. Conclusion: This model can accurately predict the prognosis of HIV complicated with Talaromyces marneffei infection.

IL-38 alleviates airway remodeling in chronic asthma via blocking the profibrotic effect of IL-36γ.

Airway remodeling is a major feature of asthma. Interleukin (IL)-36γ is significantly upregulated and promotes airway hyper-responsiveness (AHR) in asthma, but its role in airway remodeling is unknown. Here, we aimed to investigate the role of IL-36γ in airway remodeling, and whether IL-38 can alleviate airway remodeling in chronic asthma by blocking the effects of IL-36γ. IL-36γ was quantified in mice inhaled with house dust mite (HDM). Extracellular matrix (ECM) deposition in lung tissues and AHR were assessed following IL-36γ administration to mice. Airway inflammation, AHR, and remodeling were evaluated after IL-38 or blocking IL-36 receptor (IL-36R) treatment in asthmatic mice. The effects of lung fibroblasts stimulated with IL-36γ and IL-38 were quantified in vitro. Increased expression of IL-36γ was detected in lung tissues of HDM-induced asthmatic mice. The intratracheal instillation of IL-36γ to mice significantly enhanced the ECM deposition, AHR, and the number of activated lung fibroblasts around the airways. IL-38 or blocking IL-36R treated asthmatic mice showed a significant alleviation in the airway inflammation, AHR, airway remodeling, and number of activated fibroblasts around airways as compared with the HDM group. In vitro, IL-36γ promoted the activation and migration of human lung fibroblasts (HFL-1). The administration of IL-38 can counteract these biological processes induced by IL-36γ in HFL-1cells. The results indicated that IL-38 can mitigate airway remodeling by blocking the profibrotic effects of IL-36γ in chronic asthma. IL-36γ may be a new therapeutic target, and IL-38 is a potential candidate agent for inhibiting airway remodeling in asthma.

Multicentric Castleman disease of hyaline­vascular variant with paraneoplastic pemphigus results in abnormal lung function: Report of 3 cases.

Castleman disease (CD) is clinically divided into unicentric CD (UCD) and multicentric CD (MCD). Hyaline-vascular variant (HV) is the most common pathological type of UCD, while the plasma cell type (PC) is the most common type of MCD and thus, hyaline-vascular variant multicentric CD (HV-MCD) is a rare type of CD. In addition, its etiology has remained elusive. The present study retrospectively analyzed the medical records of 3 patients diagnosed as HV-MCD admitted to The First Affiliated Hospital of Guangxi Medical University (Guangxi, China) between January 2007 and September 2020. A total of 2 males and 1 female were admitted. The areas involved varied considerably. Respiratory symptoms were seen in 3 cases, along with fever, weight loss and splenomegaly. Damage to the skin and mucous membranes resulted in oral ulcers when accompanied by paraneoplastic pemphigus (PNP). Dry and wet rales were found in all patients. All 3 cases were complicated with PNP and had hypoxemia and obstructive ventilation dysfunction. In accordance with PC-MCD, it manifested as lymph node enlargement and may involve several lymph nodes. Computed tomography mainly indicated bronchiectasis and mediastinal lymph node enlargement. In 1 case, chemotherapy failed after local mass excision, 1 case remitted after chemotherapy but the lung lesion was irreversible and 1 case was untreated and soon died of respiratory failure. The cases of HV-MCD with pulmonary involvement were induced by small airway lesions and associated with poor prognosis. Respiratory symptoms along with systemic symptoms were common.

Extracranial Vertebral Artery-Internal Jugular Vein-Spinal Vein Fistula in Neurofibromatosis Type I: Case Report and Literature Review.

Background: A cervical arteriovenous fistula (AVF) in neurofibromatosis type I (NF-1) is uncommon, and it brings challenges and difficulty in treatment. Case Presentation: A 39-year-old woman was diagnosed with an NF-1-associated spontaneous vertebral artery-internal jugular vein-spinal vein fistula. The fistula was placed by coil embolization. Postoperative examination showed that the fistula closure was satisfied, and the patient's abnormal clinical manifestation disappeared without any complications after 24 months of interventional embolization. As per the literature, interventional embolization is currently the main treatment method, and it has the distinguishing features of less trauma, quick recovery, and a good prognosis. Conclusion: NF-1 associated with a spontaneous arteriovenous fistula is rare in clinical practice, which carries significant challenges in treatment, but can be effectively treated using endovascular embolism. Endovascular embolism could be the potential choice of treatment in NF-1 associated with AVF.

Suitability of 3.5-mm screw for the atlas in children: a retrospective computed tomography analysis.

BACKGROUND: The growth and development of the atlas in children has not been studied to date using a large sample size. OBJECTIVE: To study whether a 3.5-mm screw is suitable for the atlas in children, to explore the anatomical size and development of the atlas in 0-14-year-old children, and to provide morphological basis for lateral mass screw internal fixation. METHODS: A Computed Tomography (CT) morphometric analysis was performed on 420 pediatric atlases. In the atlas, D1, D2, D3, D4, and α of the atlas lateral mass were measured. Statistical analysis was performed using one-way ANOVA and Students' t test. The least square method was used for the regression analysis of the change trend in anatomical structure. The curve with the greatest goodness of fit was used as the anatomic trend regression curve. RESULTS: D1, D2, D3, and D4 generally showed an increasing trend with age. The ranges of averages of D1, D2, D3, D4, and α in 0-14 year-old children were as follows: 4.576-9.202 mm, 9.560-25.100 mm, 3.414-10.554 mm, 11.150-27.895, and 12.41°-20.97°, respectively. The trends of the fitting curves of L1 and L3 were power functions, and those of L2 and L4 were logarithmic curves. CONCLUSIONS: CT examination could help in preoperative decision-making, and 3.5-mm screw was found to be suitable for lateral mass screw internal fixation in children aging 2 years and older. D1-D4 increased with age. This provided a certain reference to perform posterior atlantoaxial fusion in children and is of great significance to design posterior atlantoaxial screw in children.

Feasibility of 3.5 mm C2 pedicle screws in children: A computerized tomography analysis.

There have been no studies with large sample sizes on growth of the pedicle of C2 in children. In the present study we measured the pedicle of C2 through computed tomography (CT) imaging in children aged less than 14 years and evaluated the suitability of the 3.5-mm screw for the pedicle in such children. The study was conducted on CT morphometric images of 420 children in our hospital between June 2018 and June 2020. The width (D1), length (D2), height (D3), inclination angle (α), and tail angle (ß) of the C2 pedicle were measured. One-way analysis of variance and Student's t test were used for statistical analyses. The least-square method was used to analyze the curve fitting the trend of anatomical change in the pedicle. The largest degree of goodness of fit determined the best-fitting curve. The size of the pedicle of C2 increased with age. The median ranges of D1, D2, D3, α, and ß were 3.312-5.431 mm, 11.732-23.645 mm, 3.597-8.038 mm, 32.583°-36.640°, and 24.867°-31.567°, respectively. The curves fitting the trends of D1 and D3 were power functions, whereas D2 was fitted by a logarithmic curve. However, no curve fitted α or ß. A 3.5-mm screw can be placed in the pedicle of C2 in children aged more than 1 year. The growth and development trend of this pedicle can provide an anatomical reference for deciding on posterior cervical surgery and for selecting and designing pedicle screws for children.

A seven-gene signature and the C-C motif chemokine receptor family genes are the sarcoma-related immune genes.

Cells of the tumor microenvironment exert a vital influence on sarcoma prognosis. This study aimed to analyze and identify differentially expressed genes (DEGs) related to immunity and their significance as immune biomarkers for the accurate prediction of overall survival of patients with sarcoma. The Cancer Genome Atlas was adopted for obtaining sarcoma gene microarray and corresponding clinical information. ESTIMATE algorithm was used to calculate tumor immune microenvironment indices. Immune-associated DEGs were identified using the limma packages and were further analyzed using the ClusterProfiler package and STRING website. Based on the results of these analyses, we constructed a prognostic model. Furthermore, we assessed the prognosis prediction model through functional evaluation and analysis of GSE17674. The functional analysis revealed that the upregulated immune DEGs were related to immune-related aspects. Chemokine ligands/receptors and immune-related genes were found to be vital for sarcoma formation and progression. We established a prognostic signature of seven genes, which indicated that high-risk cases exhibit poor prognostic outcome. The prognostic signature constructed in this study can accurately predict the overall prognosis in patients with sarcoma. Moreover, the novel immune gene expression analysis may provide clinical guidance for predicting prognosis in patients with sarcoma.

Talaromyces marneffei and nontuberculous mycobacteria co-infection in HIV-negative patients.

To describe the clinical features and the risk factors for nontuberculous mycobacteria (NTM) and Talaromyces marneffei (TM) co-infections in HIV-negative patients. A multicenter retrospective study in 13 hospitals, and a systematic literature review were performed of original articles published in English related to TM/NTM co-infections. HIV-negative patients with TM and NTM co-infections comprised Group 1; TM-only infection Group 2; NTM-only infection Group 3; and healthy volunteers Group 4. Univariate logistic analysis was used to estimate the potential risk factors of TM/NTM co-infections. A total of 22 cases of TM and NTM co-infections were enrolled. Of these, 17 patients (77.3%) had a missed diagnosis of one of the TM or NTM pathogens. The anti-IFN-γ autoantibodies (AIGAs) titer, white blood cell (WBC), neutrophil counts (N), erythrocyte sedimentation rate (ESR), C reactive protein (CRP), globulin, and immunoglobulin G (IgG) levels of Group 1 were higher than those of the other groups, whereas the levels of CD4+T cells was lower than those of other groups. There was a significant negative correlation between the AIGA titers and the number of CD4+T cells (P < 0.05). Factors including the ratio of the actual values to the cut-off values of AIGAs, WBC, N, HGB, CD4+T cells, IgG, IgM, IgA, serum globulin, ESR, and CRP were taken as potential risk factors for TM and NTM co-infection. Most patients with TM and NTM co-infection had a missed diagnosis of one of the TM or NTM pathogens. The levels of AIGAs, WBC, N, ESR, and CRP in TM and NTM co-infections were remarkably higher than in mono-infection. High-titer AIGAs may be a potential risk factor and susceptibility factor for co-infection of TM and NTM in HIV-negative hosts.

Comprehensive analyses of potential key genes in active tuberculosis: A systematic review.

BACKGROUND: Tuberculosis (TB) is a global health problem that brings us numerous difficulties. Diverse genetic factors play a significant role in the progress of TB disease. However, still no key genes for TB susceptibility have been reported. This study aimed to identify the key genes of TB through comprehensive bioinformatics analysis. METHODS: The series microarray datasets from the gene expression omnibus (GEO) database were analyzed. We used the online tool GEO2R to filtrate differentially expressed genes (DEGs) between TB and health control. Database for annotation can complete gene ontology function analysis as well as Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Protein-protein interaction (PPI) networks of DEGs were established by STRING online tool and visualized by Cytoscape software. Molecular Complex Detection can complete the analysis of modules in the PPI networks. Finally, the significant hub genes were confirmed by plug-in Genemania of Cytoscape, and verified by the verification cohort and protein test. RESULTS: There are a total of 143 genes were confirmed as DEGs, containing 48 up-regulated genes and 50 down-regulated genes. The gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis show that upregulated DEGs were associated with cancer and phylogenetic, whereas downregulated DEGs mainly concentrate on inflammatory immunity. PPI networks show that signal transducer and activator of transcription 1 (STAT1), guanylate binding protein 5 (GBP5), 2'-5'-oligoadenylate synthetase 1 (OAS1), catenin beta 1 (CTNNB1), and guanylate binding protein 1 (GBP1) were identified as significantly different hub genes. CONCLUSION: We conclude that these genes, including TAT1, GBP5, OAS1, CTNNB1, GBP1 are a candidate as potential core genes in TB and treatment of TB in the future.

Bioinformatic analysis of the pathogenic mechanism of talaromyces marneffei infection.

BACKGROUND: Talaromyces marneffei (T marneffei), known as a significant pathogen in patients with AIDS in Southeast Asia, is a dimorphic fungus, which can cause deadly systematic infection in immunocompromised hosts. What is more, the dimorphic phase transition has been reported as a conspicuous process linked with virulence. Interestingly, the yeast form was found in infected individuals, representing the pathogenic phase. However, few researches were found to study the mechanism of dimorphic transition. Thus, a diverse insight into the dimorphic switch mechanism, is urgently needed and we are the first one to research the mechanism of dimorphism. METHODS: Firstly, we investigated the microarray of T. marneffei in the Gene Expression Omnibus database (GEO) for differentially expressed genes (DEGs). Then Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.8 was employed to analyze the underlying enrichment and pathway in biological process of DEGs. Meanwhile, protein-protein interaction (PPI) network was constructed using STRING database. On the strength of the theory that similar amino acid sequences share similar structures, which play a decisive role on the function of protein, three dimensional structures of hub-genes were predicted to further investigate the likely function of hub-genes. RESULTS: GSE51109 was elected as the eligible series for the purpose of our research, including GSM1238923 (GSM23), GSM1238924 (GSM24), and GSM1238925 (GSM25). PMAA_012920, PMAA_028730, PMAA_068140, PMAA_092900, PMAA_032350 were the most remarkable genes in all of the three PPI networks, thus, were viewed as hub-genes. With regard to the three-dimensional construction, except that there was no significant prediction structure of PMAA_092900 with the criterion seq identify > 30%, GMQE: 0-1, QMEAN4: -4-0, the parallel templates for four structures were Crystal structure of Saccharomyces cerevesiae mitochondrial NADP(+)-dependent isocitrate dehydrogenase in complex with isocitrate, Organellar two-pore channels (TPCs), Yeast Isocitrate Dehydrogenase (Apo Form) and Crystal Structure Of ATP-Dependent Phosphoenolpyruvate Carboxykinase From Thermus thermophilus HB8 in order. CONCLUSION: The dimorphic transition of T. marneffei was viewed as a pathogenic factor and DEGs were observed. In-depth study of the function and pathway of DEGs revealed that PMAA_012920, PMAA_028730, PMAA_068140, PMAA_092900, PMAA_032350 were most likely acting as the hub-genes and were likely taking effect through regulating energy metabolism.

KEGG-expressed genes and pathways in triple negative breast cancer: Protocol for a systematic review and data mining.

BACKGROUND: The incidence of triple negative breast cancer (TNBC) is at a relatively high level, and our study aimed to identify differentially expressed genes (DEGs) in TNBC and explore the key pathways and genes of TNBC. METHODS: The gene expression profiling (GSE86945, GSE86946 and GSE102088) data were obtained from Gene Expression Omnibus Datasets, DEGs were identified by using R software, Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of DEGs were performed by the Database for Annotation, Visualization and Integrated Discovery (DAVID) tools, and the protein-protein interaction (PPI) network of the DEGs was constructed by the STRING database and visualized by Cytoscape software. Finally, the survival value of hub DEGs in breast cancer patients were performed by the Kaplan-Meier plotter online tool. RESULTS: A total of 2998 DEGs were identified between TNBC and health breast tissue, including 411 up-regulated DEGs and 2587 down-regulated DEGs. GO analysis results showed that down-regulated DEGs were enriched in gene expression (BP), extracellular exosome (CC), and nucleic acid binding, and up-regulated were enriched in chromatin assembly (BP), nucleosome (CC), and DNA binding (MF). KEGG pathway results showed that DEGs were mainly enriched in Pathways in cancer and Systemic lupus erythematosus and so on. Top 10 hub genes were picked out from PPI network by connective degree, and 7 of top 10 hub genes were significantly related with adverse overall survival in breast cancer patients (P < .05). Further analysis found that only EGFR had a significant association with the prognosis of triple-negative breast cancer (P < .05). CONCLUSIONS: Our study showed that DEGs were enriched in pathways in cancer, top 10 DEGs belong to up-regulated DEGs, and 7 gene connected with poor prognosis in breast cancer, including HSP90AA1, SRC, HSPA8, ESR1, ACTB, PPP2CA, and RPL4. These can provide some guidance for our research on the diagnosis and prognosis of TNBC, and further research is needed to evaluate their value in the targeted therapy of TNBC.

Expression of microRNA-99a-3p in Prostate Cancer Based on Bioinformatics Data and Meta-Analysis of a Literature Review of 965 Cases.

BACKGROUND microRNAs (miRNAs) have a role as biomarkers in human cancer. The aim of this study was to use bioinformatics data, and review of cases identified from the literature, to investigate the role of microRNA-99a-3p (miR-99a-3p) in prostate cancer, including the identification of its target genes and signaling pathways. MATERIAL AND METHODS Meta-analysis from a literature review included 965 cases of prostate cancer. Bioinformatics databases interrogated for miR-99a-3p in prostate cancer included The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO), and ArrayExpress. Twelve computational predictive algorithms were developed to integrate miR-99a-3p target gene prediction data. Bioinformatics analysis data from Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) network analysis were used investigate the possible pathways and target genes for miR-99a-3p in prostate cancer. RESULTS TCGA data showed that miR-99a was down-regulated in prostate cancer when compared with normal prostate tissue. Receiver-operating characteristic (ROC) curve area under the curve (AUC) for miR-99a-3p was 0.660 (95% CI, 0.587-0.732) or a moderate level of discriminations. Pathway analysis showed that miR-99a-3p was associated with the Wnt and vascular endothelial growth factor (VEGF) signaling pathways. The PPP3CA and HYOU1 genes, selected from the PPI network, were highly expressed in prostate cancer tissue compared with normal prostate tissue, and negatively correlated with the expression of miR-99a-3p. CONCLUSIONS In prostate cancer, miR-99a-3p expression was associated with the Wnt and VEGF signaling pathways, which might inhibit the expression of PPP3CA or HYOU1.

LncRNA NEAT1 Promotes Deterioration of Hepatocellular Carcinoma Based on In Vitro Experiments, Data Mining, and RT-qPCR Analysis.

BACKGROUND/AIMS: Accumulated evidence indicates that lncRNA NEAT1 has important roles in various malignant tumors. In this study, we conducted a comprehensive analysis to explore the exact role of NEAT1 in hepatocellular carcinoma (HCC). METHODS: The effects of NEAT1 on cell proliferation, apoptosis, migration, and invasion were measured by in vitro experiments. The expression level and clinical value of NEAT1 in HCC was evaluated based on data from The Cancer Genome Atlas (TCGA), Oncomine, and in-house real-time quantitative (RT-qPCR). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) network analyses were conducted to investigate the potential molecular mechanisms of NEAT1. RESULTS: NEAT1 siRNA not only inhibited proliferation, migration, and invasion of HCC cells but also induced HCC cell apoptosis. A total of four records from TCGA, Oncomine, and RT-qPCR analysis were combined to assess the expression level of NEAT1 in HCC. The pooled standard mean deviation (SMD) indicated that NEAT1 was up-regulated in HCC (SMD = 0.54; 95% CI, 0.36-0.73; P < 0.0001). The area under the curve value of the summary receiver operating characteristic curve was 0.71. NEAT1 expression was also related to race (P = 0.025) and distant metastasis (P = 0.002). Additionally, the results of GO, KEGG pathway, and PPI network analyses suggest that NEAT1 may promote the progression of HCC by interacting with several tumor-related genes (SP1, MDM4, CREBBP, TRAF5, CASP8, TRAF1, KAT2A, and HIST4H4). CONCLUSIONS: NEAT1 contributes to the deterioration of HCC and provides a potential biomarker for the diagnosis and therapy of HCC.

Clinical Significance of miR-210 and its Prospective Signaling Pathways in Non-Small Cell Lung Cancer: Evidence from Gene Expression Omnibus and the Cancer Genome Atlas Data Mining with 2763 Samples and Validation via Real-Time Quantitative PCR.

BACKGROUND/AIMS: Since the function of microRNA (miR)-210 in non-small cell lung cancer (NSCLC) remains unclear, we aimed to explore the clinical significance of miR-210 in NSCLC. METHODS: NSCLC-related data from 1673 samples on Gene Expression Omnibus and 1090 samples on The Cancer Genome Atlas were obtained and analyzed. The expression level of miR-210 was validated via real-time quantitative PCR analysis with 125 paired clinical samples. A meta-analysis was performed to generate a comprehensive understanding of miR-210 expression and its clinical significance in NSCLC. In addition, bioinformatics analysis was also conducted to reveal the potential underlying mechanism of miR-210 action in NSCLC. RESULTS: miR-210 expression was consistently elevated in NSCLC solid tissue samples. However, its expression was controversial in easily obtained body fluids (i.e., blood, plasma, and serum). Moreover, an overall pooled meta-analysis implied a comparatively higher level of miR-210 expression in NSCLC cancerous tissue than in normal control tissue (P < 0.001). In addition, a meta-analysis of outcome revealed a significant diagnostic capacity of miR-210 in NSCLC by detecting its expression in serum and sputum (area under the summary receiver operating characteristic curve 0.82 and 0.81, respectively). miR-210 overexpression was associated with poor progression-free survival (PFS) in NSCLC and was negatively related to overall survival and disease-free survival. Bioinformatic gene enrichment and annotation analyses showed that the target genes of miR-210 were greatly enriched in cell adhesion and plasma membrane, and three pathways were considered to be the main functional circuits of miR-210: renin secretion, the cGMP-PKG signaling pathway, and cell adhesion molecules. CONCLUSION: In NSCLC, miR-210 expression was elevated and overexpression indicated poor PFS. Expression level of miR-210 in serum and sputum showed significant diagnostic value for NSCLC.

Diagnostic value of strand-specific miRNA-101-3p and miRNA-101-5p for hepatocellular carcinoma and a bioinformatic analysis of their possible mechanism of action.

There is accumulating evidence that miRNA might serve as potential diagnostic and prognostic markers for various types of cancer. Hepatocellular carcinoma (HCC) is the most common type of malignant lesion but the significance of miRNAs in HCC remains largely unknown. The present study aimed to establish the diagnostic value of miR-101-3p/5p in HCC and then further investigate the prospective molecular mechanism via a bioinformatic analysis. First, the miR-101 expression profiles and parallel clinical parameters from 362 HCC patients and 50 adjacent non-HCC tissue samples were downloaded from The Cancer Genome Atlas (TCGA). Second, we aggregated all miR-101-3p/5p expression profiles collected from published literature and the Gene Expression Omnibus and TCGA databases. Subsequently, target genes of miR-101-3p and miR-101-5p were predicted by using the miRWalk database and then overlapped with the differentially expressed genes of HCC identified by natural language processing. Finally, bioinformatic analyses were conducted with the overlapping genes. The level of miR-101 was significantly lower in HCC tissues compared with adjacent non-HCC tissues (P < 0.001), and the area under the curve of the low miR-101 level for HCC diagnosis was 0.925 (P < 0.001). The pooled summary receiver operator characteristic (SROC) of miR-101-3p was 0.86, and the combined SROC curve of miR-101-5p was 0.80. Bioinformatic analysis showed that the target genes of both miR-101-3p and miR-101-5p are involved in several pathways that are associated with HCC. The hub genes for miR-101-3p and miR-101-5p were also found. Our results suggested that both miR-101-3p and miR-101-5p might be potential diagnostic markers in HCC, and that they exert their functions via targeting various prospective genes in the same pathways.