MOLECULAR AND CELLULAR PROBES
·
2025
·
IF 3
Xin Song,Sihao Chen,Junning Cheng,Haiyu Li,Ruixin Wu,Min Yan,Min Wang,Jie Li,Aishun Jin,Wang Wang
Purpose Osteosarcoma (OS) exhibits limited immune cell infiltration that directly contributes to poor prognosis. This study sought to screen and identify pivotal biomarkers of OS immune infiltration and early diagnosis of OS. Methods The immune cell infiltration profiles with transcriptome sequencing data from 88 OS samples were explored with CIBERSORT algorithm. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Protein-protein interaction (PPI) network analyses were applied to identify hub genes, with the expressions confirmed by dual immunofluorescence in 50 OS samples. The new biomarker gene HTRA1 were examined by immunohistochemistry and validated by the Immune score and immune gene expression profile analyses. The impact of HTRA1 on OS prognosis was verified by Least absolute shrinkage and selection operator (LASSO) regression analysis. The biological effect of HTRA1 was characterized in MG63 cells. Result CD8 + T cells, activated memory CD4 + T cells and plasma cells were positively correlated with the prognosis of OS. Hub genes CCL5 , CXCL9 , CXCL13 , and HTRA1 , exhibited positive correlation with the infiltration of both CD8 + T cells and CD4 + T cells. HTRA1 expression was reduced in osteosarcoma tissues, which was positively correlated with immune scores and the expressions of immune-related genes. High levels of HTRA1 were associated with favorable OS prognosis, and could negatively impacted MG63 malignant characteristics. Conclusion CCL5 , CXCL9 , CXCL13, and HTRA1 were OS hub genes positively correlate with CD8 + T cell and CD4 + T cell infiltrations. HTRA1 can serve as an underlying biomarker for the prognosis and immunotherapy of OS.
研究领域:
肿瘤学
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免疫学
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生物信息学
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产品关联
DOI
PubMed
高影响因子
Acta Biomaterialia
·
2025
·
IF 9.6
Cheng Zeng,Xiaojing Chen,Mingxi Lin,Yizi Jin,Qing Guo,Teng Zhou,Xingang Wang,Yiping Li,Xinghui Wang,Yongming Han,Ling Du,Qianyun Tang,Peifeng Liu,Jian Zhang
The extracellular matrix (ECM) of solid tumor constitutes a formidable physical barrier that impedes immune cell infiltration, contributing to immunotherapy resistance. Breast cancer, particularly triple-negative breast cancer (TNBC), is characterized by a collagen-rich tumor microenvironment, which is associated with T cell exclusion and poor therapeutic outcomes. Discoidin domain receptor 2 (DDR2) and integrins, key ECM regulatory receptors on cancer cells, play pivotal role in maintaining this barrier. In this study, we developed a dual-receptor-targeted strategy using metal-organic frameworks (MOFs) to deliver DDR2-specific siRNA (siDDR2) and ITGAV-specific siRNA (siITGAV) to disrupt the ECM barrier. siDDR2 modulates immune infiltration by regulating collagen–cell interactions, while siITGAV suppresses TGF-β1 activation. The MOF@siDDR2+siITGAV complex significantly reduced collagen deposition, enhanced CD8+ T cell infiltration, and downregulated programmed cell death ligand 1 (PD-L1) expression in TNBC. Consequently, this approach markedly inhibited tumor growth. Our findings demonstrate that dual-receptor-targeted MOF-based nanocarriers (MOF@siDDR2+siITGAV) can effectively reprogram the tumor ECM to enhance immune cell access, offering a promising prospect for synergistic cancer immunotherapy. Statement of significance A dual-receptor-targeted MOF nanocarrier is developed to improve immune accessibility in tumors. Concurrent blockade of DDR2 and ITGAV effectively decreases collagen deposition, increases CD8+ T cell infiltration, and suppresses PD-L1 expression. Modulating the mechanical properties of the extracellular matrix (ECM) to enhance immune accessibility offers an innovative strategy for cancer treatment.
研究领域:
肿瘤学
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分子生物学
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纳米医学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Endocrinology
·
2023
·
IF 5.2
Chengxin Li,Lewei Zheng,Gaoran Xu,Qianqian Yuan,Ziyang Di,Yalong Yang,Xingxing Dong,Jinxuan Hou,Gaosong Wu
Background Breast cancer (BRCA) has become the most diagnosed cancer worldwide for female and seriously endanger female health. The epithelial-mesenchymal transition (EMT) process is associated with metastasis and drug resistance in BRCA patients. However, the prognostic value of EMT-related lncRNA in BRCA still needs to be revealed. The aim of this study is to construct an EMT-related lncRNA (ERL) signature with accuracy predictive ability for the prognosis of BRCA patients. Methods RNA-seq expression data and Clinical characteristics obtained from the TCGA (The Cancer Genome Atlas) were used in the study. First, we identified the EMT-related lncRNA by the Pearson correlation analysis. An EMT-related lncRNAs prognostic risk signature was constructed using univariate Cox regression and Lasso-penalized Cox regression analyses. The model’s performance was validated using Kaplan-Meier (KM) survival analysis, ROC curve and C-index. Finally, a nomogram was constructed for clinical practice in evaluating the patients with BRCA and validated by calibration curve and decision curve analysis (DCA). We also evaluated the drug sensitivity of signature lncRNA and the tumor immune cell infiltration in breast cancer. Results We constructed a 10-lncRNA risk score signature based on the lncRNAs associated with the EMT process. We could assign BRCA patients to the high- and low-risk group according to the median risk score. The prognostic risk signature showed excellent accuracy and demonstrated sufficient independence from other clinical characteristics. The immune cell infiltration analysis showed that the prognostic risk signature was related to the infiltration of the immune cell subtype. Drug sensitivity analysis proved ERLs signature could effectively predict the sensitivity of patients to common chemotherapy drugs in BRCA and provide guidance for chemotherapy drugs for high-risk and low-risk patients. Conclusion Our ERL signature and nomogram have excellent prognostic value and could become reliable tools for clinical guidance.
研究领域:
肿瘤学
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分子生物学
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生物信息学
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临床研究
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产品关联
DOI
PubMed
高影响因子
WORLD JOURNAL OF GASTROENTEROLOGY
·
2023
·
IF 4.3
Heng Shi,Xin-Hai Zhao,Qin Peng,Xian-Ling Zhou,Si-Si Liu,Chuan-Chuan Sun,Qiu-Yu Cao,Shi-Ping Zhu,Sheng-Yun Sun
BACKGROUND Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer known to cause liver injury. Green tea is reported to exert therapeutic effects on heavy metal exposure-induced organ damage. However, limited studies have examined the therapeutic effects of green tea polyphenols (GTPs) on DEHP-induced liver damage. AIM To evaluate the molecular mechanism underlying the therapeutic effects of GTPs on DEHP-induced liver damage. METHODS C57BL/6J mice were divided into the following five groups: Control, model [DEHP (1500 mg/kg bodyweight)], treatment [DEHP (1500 mg/kg bodyweight) + GTP (70 mg/kg bodyweight), oil, and GTP (70 mg/kg bodyweight)] groups. After 8 wk, the liver function, blood lipid profile, and liver histopathology were examined. Differentially expressed micro RNAs (miRNAs) and mRNAs in the liver tissues were examined using high-throughput sequencing. Additionally, functional enrichment analysis and immune infiltration prediction were performed. The miRNA-mRNA regulatory axis was elucidated using the starBase database. Protein expression was evaluated using immunohistochemistry. RESULTS GTPs alleviated DHEP-induced liver dysfunction, blood lipid dysregulation, fatty liver disease, liver fibrosis, and mitochondrial and endoplasmic reticulum lesions in mice. The infiltration of macrophages, mast cells, and natural killer cells varied between the model and treatment groups. mmu-miR-141-3p (a differentially expressed miRNA), Zcchc24 (a differentially expressed mRNA), and Zcchc24 (a differentially expressed protein) constituted the miRNA-mRNA-protein regulatory axis involved in mediating the therapeutic effects of GTPs on DEHP-induced liver damage in mice. CONCLUSION This study demonstrated that GTPs mitigate DEHP-induced liver dysfunction, blood lipid dysregulation, fatty liver disease, and partial liver fibrosis, and regulate immune cell infiltration. Additionally, an important miRNA-mRNA-protein molecular regulatory axis involved in mediating the therapeutic effects of GTPs on DEHP-induced liver damage was elucidated.
研究领域:
毒理学
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药理学
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分子生物学
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免疫学
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产品关联
DOI
PubMed
高影响因子
ACS Applied Polymer Materials
·
2020
·
IF 0
Chen Shen,Yujie Gao,Jun Li,Hongyao Du,Ruijing Liang,Yanhong Sun,Jun Xie,Liyun Dong,Yamin Zhang,Jinjin Zhu,Bo Zhang,Guanxin Shen,Xiang Chen,Jintao Zhu,Juan Tao
Branched polyethylenimine (BPEI) is a cationic polymer and has been applied as an antigen carrier in vaccines. However, its intrinsic adjuvanticity and underlying mechanism remain unclear. Here, we systematically explored the direct stimulation effects of a series of BPEI on bone-marrow-derived dendritic cells (BMDCs) in vitro. Only high concentrations of BPEI with molecular weight (MW) equal to or greater than 25 kDa showed an immune-activating effect, indicating that both MW and cationic degree contribute to this effect. In a charge neutralization experiment, the intrinsic adjuvanticity of BPEI also demonstrated a cationic degree-dependent pattern. Moreover, we identified reactive oxygen species (ROS) as the crucial messengers in BPEI-mediated BMDC activation. However, high MW and cationic charges from the BPEI exerted a direct toxicity on dendritic cells, which would restrict its in vivo applications. Therefore, we introduced fibroblasts as bystander cells and found that BPEI-treated fibroblasts passed stimulation effects to BMDCs with undetectable cytotoxicity. During subcutaneous stimulation, which corresponded to the fibroblast-mediated coculture system, BPEI induced an inflammatory microenvironment and local immune cell infiltration without obvious cell death. To the best of our knowledge, this is the first systematic and incisive investigation of BPEI’s intrinsic adjuvanticity and its functional exploration in the presence of bystander cells. This finding paves the way to advance the BPEI-based vaccines and will give insights into the use of other immunoactive biomaterials with similar properties.
研究领域:
免疫学
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药剂学
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生物医学工程
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DOI
JOURNAL OF GENE MEDICINE
·
2024
·Vol. 26
·期 10
·e3742
·
IF 3.2
Fuyun Zhu,Dezeng Zou,Ping Shi,Lianhua Tang,Dan Wu,Xiaoxue Hu,Fei Yin,Jianhui Liu
Background With its rapidly increasing incidence and prevalence, ulcerative colitis (UC) has become a major global health challenge. Recent evidence suggests that ferroptosis plays a significant role in the development of UC. However, the relationship between ferroptosis and the progression of UC needs to be extensively studied. Methods The differentially expressed genes in UC patients were screened from the GEO database. The ferroptosis-related genes were obtained from FErrDB and GeneCards. The UC subtypes were identified with the R package “CancerSubtype” and evaluated with consensus clustering (CC) to identify gene expression patterns in patients with UC. The key genes were detected with qRT-PCR, Western blot, and immunohistochemistry in vitro and in vivo models. Ferroptosis was identified with western blotting on ferrotic-associated proteins and staining on Fe 2+ with commercial FerroOrange kits. Results Dipeptidyl peptidase 4 (DPP4), also known as CD26, is a potential biomarker for ferroptosis in UC patients. Transcriptome sequencing data showed a positive correlation between decreased DPP4 expression and proinflammatory cytokines such as TNF-α, IL-6, and IL-β, as well as immune cell infiltration in the colon tissues of UC patients. Furthermore, DPP4 was strongly associated with ferroptosis biomarkers, particularly in Subtype 2 of UC. Interestingly, our study also found that DPP4 expression was significantly reduced in RSL3-treated ferroptotic intestinal epithelial cells, more so than in LPS-treated cell models. Inhibition of DPP4 had a significant impact on the expression of ferroptotic biomarkers. Additionally, DPP4 expression was decreased in the colon tissues of DSS-treated mice, and the ferroptosis inhibitor Ferritin-1 effectively counteracted the effects of DSS on immune cell infiltration, colon length, and DPP4 expression. Conclusions DPP4 can serve as a biomarker for ferroptosis in the diagnosis and management of UC. Highlights DPP4-mediated ferroptosis is involved in ulcerative colitis DPP4 is a novel diagnostic biomarker of ulcerative colitis Ferroptosis involves intestinal epithelial cell death in ulcerative colitis
研究领域:
胃肠病学
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分子生物学
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免疫学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Oncology
·
2025
·
IF 3.3
Chen Dai,Rishun Su,Zhenzhen Zhao,Yangyang Guo,Wenbin Hou,Yulong He,Guangyao Liu,Songcheng Yin,Changhua Zhang
Background Gastric cancer (GC) is a very aggressive, with extreme heterogeneity and rapid growth, most frequently manifested histologically as stomach adenocarcinoma (STAD). Current evidence suggests that histone acetylation is critical for the origin and development of tumors. However, the significance of histone acetylation-related gene signatures for prognosis of STAD patients and mechanisms of histone acetylation in STAD therapy remains unclear. Methods We identified histone acetylation-related genes in STAD from TCGA and constructed eight-gene signatures by utilizing a univariate Cox regression model with the Least Absolute Shrinkage and Selection Operator (LASSO). In addition, a nomogram was plotted to predict the prognostic significance of the established risk model. We examined associations between our gene signature and somatic mutation, immune subtype, clinicopathological features, tumor microenvironment, immune cell infiltration and immune activity, immunotherapy prediction and drug sensitivity. Cell-based assays were performed to determine the relationship between Doublecortin Like Kinase 1 (DCLK1) and the proliferation, migration and oxaliplatin resistance of GC cells in vitro . Immunohistochemical experiments were used to explore the relationship between DCLK1 and clinicopathological parameters. Results A prognostic model composed of eight histone acetylation-related genes in STAD was developed. Based on median risk score, the STAD patients were equally assigned into two groups of high- and low-risk, where high-risk represented a less favorable prognosis than low-risk. The two groups showed significant differences with respect to somatic mutation, immune subtype, clinicopathological features, tumor microenvironment, immune cell infiltration and immune activity, immunotherapy prediction and drug sensitivity. The results generated during Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses suggested that Differentially Expressed Genes (DEGs) in the two groups were involved in cancer-related processes and pathways. Cell-based assays indicated that DCLK1 is a promoting factor in gastric cancer and can promote oxaliplatin resistance in gastric cancer cells. Increased DCLK1 expression was also associated with Borrmann’s Type, depth of invasion, lymph node metastasis, and TNM stage in GC patients. Conclusion A novel histone acetylation-related gene signature, which possesses potential value in predicting the prognosis and immunotherapy effectiveness regarding STAD patients, was developed. This signature may serve as a reliable biomarker for prognosis of STAD and promote the identification of novel treatment targets for STAD. Furthermore, DCLK1 exhibited oncogenic roles and may be a new target for STAD therapy.
研究领域:
肿瘤学
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分子生物学
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免疫治疗
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生物信息学
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癌症基因组学
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产品关联
DOI
PubMed
高影响因子
Small
·
2022
·Vol. 19
·期 9
·2205531
·
IF 15.153
Qian-Wei Luo,Lu Yao,Ling Li,Zhuo Yang,Mei-Mei Zhao,Yong-Zhe Zheng,Fang-Fang Zhuo,Ting-Ting Liu,Xiao-Wen Zhang,Dan Liu,Peng-Fei Tu,Ke-Wu Zeng
Understanding the direct interaction of nanostructures per se with biological systems is important for biomedical applications. However, whether nanostructures regulate biological systems by targeting specific cellular proteins remains largely unknown. In the present work, self-assembling nanomicelles are constructed using small-molecule oleanolic acid (OA) as a molecular template. Unexpectedly, without modifications by functional ligands, OA nanomicelles significantly activate cellular proteasome function by directly binding to 20S proteasome subunit alpha 6 (PSMA6). Mechanism study reveals that OA nanomicelles interact with PSMA6 to dynamically modulate its N-terminal domain conformation change, thereby controlling the entry of proteins into 20S proteasome. Subsequently, OA nanomicelles accelerate the degradation of several crucial proteins, thus potently driving cancer cell pyroptosis. For translational medicine, OA nanomicelles exhibit a significant anticancer potential in tumor-bearing mouse models and stimulate immune cell infiltration. Collectively, this proof-of-concept study advances the mechanical understanding of nanostructure-guided biological effects via their inherent capacity to activate proteasome.
研究领域:
纳米技术
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癌症生物学
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分子生物学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
HUMAN MUTATION
·
2025
·Vol. 2025
·期 1
·5319444
·
IF 3.7
Xin Wu,Linde Sun,Peifa Liu,Qiong Wang,Yu Wang
Background PANoptosis, as an inflammatory programmed cell death, is involved in tumor development. This study set out to discover novel PANoptosis-correlated prognostic signatures in stomach adenocarcinoma (STAD), a prevalent malignancy of the digestive system. Methods STAD samples were derived from a public database, and PANoptosis-related genes (PRGs) were acquired from existing reports. Prognosis-related PRGs were screened by univariate Cox regression analysis. Molecular subtypes of STAD were identified by the “ConsensusClusterPlus” package. The “Limma” package was employed to filter differentially expressed genes (DEGs) between different subtypes. PANoptosis-related prognostic signatures in STAD were identified to establish the RiskScore model. The RiskScore and some of the clinical features were integrated to establish a nomogram. Immune cell infiltration and TIDE score in different risk groups were compared. Correlation between immune checkpoint genes, drug sensitivity, and RiskScore was analyzed by the Spearman method. The biological function of PANoptosis-related signature genes in STAD was preliminarily explored by in vitro cell experiments. Results Based on 18 prognosis-related PRGs, two molecular subtypes of STAD were recognized, and the C1 subtype showed a lower overall survival (OS) rate than the C2 subtype. Further, three PANoptosis-related signature genes ( APOD , GPC3 , and SERPINE1 ) were determined to establish a RiskScore model that could accurately assess the prognostic outcomes for STAD patients. Then, by integrating RiskScore with clinical features, a nomogram was established. The high-risk group had higher immune cell infiltration and TIDE score and lower OS rate than those with a low risk. RiskScore was positively correlated with nine immune checkpoint genes. Besides, we screened 23 drugs that significantly correlated with RiskScore. In vitro cell experiments showed that the mRNA and protein levels of APOD , GPC3 , and SERPINE1 were upregulated in the STAD cell line and that APOD knockout significantly reduced cancer cell proliferation, migration, and invasion levels and increased the apoptotic capacity of the STAD cell line. Conclusion This study established a PANoptosis-related RiskScore model for assessing STAD patient prognosis, which could contribute to the personalized treatment of STAD.
研究领域:
肿瘤学
·
分子生物学
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生物信息学
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免疫治疗
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精准医学
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DOI
PubMed
高影响因子
CARCINOGENESIS
·
2023
·
IF 4.7
Han Sijia,Jin Xueying,Hu Tianyu,Chi Feng
Downregulation of ARHGAP25 was found in the tumor samples from breast cancer patients and five breast cancer cell lines. However, its precise role and molecular mechanisms in breast cancer remain completely unknown. Herein, we found that knockdown of ARHGAP25 in breast cancer cells promoted proliferation, migration and invasion of breast cancer cells. Mechanistically, ARHGAP25 silence facilitated the activation of the Wnt/β-catenin pathway and the upregulation of its downstream molecules (including c-Myc, Cyclin D1, PCNA, MMP2, MMP9, Snail, and ASCL2) by directly regulating Rac1/PAK1 in breast cancer cells. In vivo xenograft experiments indicated ARHGAP25 silence promoted tumor growth and activated the Wnt/β-catenin pathway. In contrast, overexpression of ARHGAP25 in vitro and in vivo impeded all of the above cancer properties. Intriguingly, ASCL2, a downstream target of the Wnt/β-catenin pathway, transcriptionally repressed the expression of ARHGAP25 and therefore constituted a negative feedback loop. Moreover, bioinformatics analysis indicated that ARHGAP25 is significantly correlated with tumor immune cell infiltration and the survival of patients with different immune cell subgroups in breast cancer. Collectively, our work revealed that ARHGAP25 suppressed tumor progression of breast cancer. It provides a novel insight for the treatment of breast cancer.
研究领域:
肿瘤学
·
分子生物学
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细胞生物学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
NEUROCHEMICAL RESEARCH
·
2024
·Vol. 50
·期 1
·1-15
·
IF 3.7
Luo Yuanfei,Yuan Linying,Liu Zhihui,Dong Weichen,Huang Li,Liao Anyu,Xie Yi,Liu Rui,Lan Wenya,Cai Yulong,Zhu Wusheng
Proprotein convertase substilin/kexin type 9 (PCSK9), a pivotal protein regulating lipid metabolism, has been implicated in promoting microthrombotic formation and inflammatory cascades, thereby contributing to cardiovascular ischemia/reperfusion (I/R) injury. However, its involvement in cerebral I/R injury and its potential role in microcirculation protection remain unexplored. In this investigation, we utilized a middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model to simulate ischemic stroke. Different concentrations of evolocumab (1, 5, 10 mg/kg, i.v.), a PCSK9 inhibitor, were administered to assess its impact. Immunofluorescence staining was employed to analyze changes in the expression of occludin, claudin-5, thrombocyte, ICAM-1, VCAM-1, and CD45, providing insights into blood-brain barrier integrity, platelet adhesion, and immune cell infiltration. Moreover, the Morris water maze and elevated plus maze were utilized to evaluate neurological and behavioral functions in MCAO/R mice, shedding light on the effects of PCSK9 inhibition. Our findings revealed a surge in plasma PCSK9 levels post-MCAO/R, peaking at 24 h post-reperfusion. Evolocumab (10 mg/kg) treatment significantly mitigated brain infarction and neurological deficits, evidenced by enhanced locomotor function and reduced post-stroke anxiety. However, it did not ameliorate cognitive impairment following MCAO/R. Additionally, evolocumab administration led to diminished leakage of evans blue solution and upregulated expression of occludin and claudin-5. Thrombocyte, ICAM-1, VCAM-1, and CD45 levels were notably reduced in the penumbral area post-evolocumab treatment. These protective effects are speculated to be mediated through the inhibition of the ERK/NF-κB pathway. The PCSK9 inhibitor evolocumab holds promise as a therapeutic agent during the acute phase of stroke, exerting its beneficial effects by modulating the ERK/NF-κB signaling pathway.
研究领域:
神经科学
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药理学
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心血管研究
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免疫学
✓ 已验证
DOI
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Shuangjun Li,Ruyue Shi,Yankun Liu,Mingcong Niu,Zhicun Liu,Zhongjuan Wang,Jiwang Gao,Hongda Cai,Zhuyu Zhou,Shengnan Li,Xiuhua Zhao
Immune cells infiltrating tumors play a pivotal role in tumor progression regulation; however, their functionality is frequently suppressed by the acidic conditions of the tumor microenvironment (TME). Targeting and reversing tumor acidity holds significant potential for enhancing the efficacy of immunotherapy. Here, we present a proof-of-concept study on tumor acidity-reversal therapy mediated by bacterial cellulose-targeted micelles to promote M2 macrophage repolarization to M1 macrophages and restore the anti-tumor function of T cells. Our strategy utilizes a bacterial cellulose (BC) composite modified with folic acid (FA) and chrysin (BY), loaded with lactic acid-neutralizing chemotherapeutic vincristine (VCR) and lactate dehydrogenase inhibitor GNE-140, to self-assemble into tumor-targeted nanoparticles. Post-treatment, FA-BC-BY@VCR@GNE-140 demonstrated notable efficacy in reversing tumor acidity, inducing tumor cell death, mitigating immunosuppression, and stimulating host adaptive immunity. This approach represents an innovative strategy for synergizing chemotherapy and immunotherapy to combat tumor progression.
研究领域:
肿瘤免疫学
·
纳米医学
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药物递送
·
肿瘤微环境
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免疫治疗
·
生物材料
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）