Collagen and Leather
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2025
·Vol. 7
·期 1
·42
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IF 9.2
Yi Xueling,Luo Duanyang,Liu Siqi,Chen Yanxu,Guo Jin,Yan Qingyu,Mao Hui
Antibiotic contamination has been a concerning environmental issue due to its potential threats to the development of drug-resistant bacteria and genes. Plant polyphenols were employed as biomolecule chelating ligands to graft onto collagen fibers, followed by the chelative immobilization of Fe ions. The as-obtained environmentally benign chelative biosorbent (CFBT-Fe) features a classic fibrous structure, excellent distribution and reservation of Fe ions, increased thermal stability, and inhibited swelling behavior owing to the introduction of bayberry tannin. An exceptional adsorption capacity of tetracycline on CFBT-Fe is exhibited across a broad pH range (3.0–10.0). Optimal adsorption capacity (31.30 mg/g) occurs at neutral pH 7.0, which is higher than many other similar biosorbents reported in the literature. The CFBT-Fe exhibits exceptional recyclability with sixth-cycle adsorption performance at 25.27 mg/g. The environmentally benign coordinative biosorbent is considered a promising candidate for the effective adsorptive removal of tetracycline from aquatic environments across a wide pH range. Graphical
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Probiotics and Antimicrobial Proteins
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2025
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IF 4.4
Huang Xi,Gao Zhangshan,Gao Peichao,Ji Helong,Xu Laizhi,Fan Wentao,Song Suquan
Intensive poultry farming has significantly increased the incidence of lipid metabolic disorders, severely compromising the economic benefits of poultry industry. Currently, gamma-aminobutyric acid (GABA) is primarily used to mitigate adverse effects of heat stress in poultry, while the effects and mechanisms of GABA on lipid metabolism disorders remain underexplored. Lactobacillus plantarum ( L. plantarum ) serves as a significant source of GABA and is widely used in the livestock industry. This study therefore examines the effects of postbiotic GABA and the GABA-producing probiotic L. plantarum 1-2-3 on abdominal adipose tissue of laying hens following corticosterone-induced stress. To this end, hens subjected to corticosterone subcutaneous injections (4 mg/kg of body weight) were respectively received GABA (100 mg/kg BW) or L. plantarum 1-2-3 (1 × 10⁹ CFU/day). Results demonstrated that both GABA and L. plantarum 1-2-3 alleviated corticosterone-induced lipid metabolism disorders and reduced adipocyte size in abdominal fat. Additionally, expression analyses of genes and proteins related to lipid metabolism (PPARγ, C/EBPα, CD36, LPL, ATGL, and HSL) further showed that GABA and L. plantarum 1-2-3 inhibited excessive deposition of abdominal lipids in laying hens by suppressing adipogenesis and lipogenesis, while promoting lipolysis. Moreover, GABA and L. plantarum 1-2-3 both mitigated lipid deposition-induced inflammation and oxidative damage by normalizing macrophage infiltration and improving antioxidative enzyme activities (GSH-Px, T-SOD, CAT). These findings demonstrate the efficacy of GABA and L. plantarum 1-2-3 in alleviating lipid metabolism disorders in the abdominal adipose tissue of laying hens, suggesting their promise as nutritional supplements for counteracting stress-induced metabolic dysfunction.
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Phenomics
·
2025
·
IF 6.2
Hu Hongye,Wu Yanzhi,Hong Jingwei,Wang Huiying,Zhang Xiaohua,Huang Guanli,Zhu Xiaofang
Breast cancer (BC) remains the predominant form of cancer among women. Arsenic trioxide (ATO), an element in traditional Chinese medicine, has shown potential for treating BC, particularly when combined with resveratrol. However, the exact mechanisms of their combined action are not fully understood. This study aims to clarify their combined mechanisms through network pharmacology and experimental validation. In vitro experiments confirmed that compared with either agent alone, the combination of ATO and resveratrol more effectively inhibited the production of estrogen receptor 1 ( ESR1 ), tumor protein P53 ( TP53 ), and v-AKT murine thymoma viral oncogene homolog 1 ( AKT1 ) in MCF-7 cells. Our findings indicate that the combination of ATO and resveratrol significantly promotes cell apoptosis by suppressing ESR1 , TP53 , and AKT1 . Thus, ATO and resveratrol together may offer a promising strategy for BC treatment.
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Nature Communications
·
2025
·Vol. 16
·期 1
·11509
·
IF 15.7
Chen Yigang,Ji Xiang,Zhang Ziyue,Zhu Zihao,Zhou Yuming,Su Chang,Lin Yang-Chi-Dung,Huang Hsi-Yuan,Wei Kangping,Lai Yi,Chen Ke,Lin Xingqiao,Zhang Yangyi,Fu Jiehui,Huang Yixian,Cui Shidong,Yen Shih-Chung,Zhang Tao,Warshel Arieh,Huang Hsien-Da
Deep learning-based drug-target interaction (DTI) prediction methods have demonstrated strong performance; however, real-world applicability remains constrained by limited data diversity and modeling complexity. To address these challenges, we propose SCOPE-DTI, a unified framework combining a large-scale, balanced semi-inductive human DTI dataset with advanced deep learning modeling. SCOPE-DTI is constructed from 13 public repositories and expands data volume by up to 100-fold compared to common benchmarks such as the Human dataset. The SCOPE model integrates three-dimensional protein and compound representations, graph neural networks, and bilinear attention mechanisms to effectively capture cross domain interaction patterns and outperform state-of-the-art methods across various DTI prediction tasks. Additionally, SCOPE-DTI provides a user-friendly interface and database. We further demonstrate its effectiveness by experimentally identifying anticancer targets of two bioactive natural compounds. By offering comprehensive data, advanced modeling, and accessible tools, SCOPE-DTI accelerates drug discovery research.
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Cell Death & Disease
·
2025
·
IF 9.6
Huang Hongli,Chai Yihan,Wu Xuewei,Wang Sen,Li Binglin,Wang Yanyan,Zheng Wen,Wu Yuefeng,Meng Di,Wang Hua,Tu Zhengliang,Du Chengli,Lyu Xiayi,Li Guiying,Guo Wei
Non-genetic resistance of cancer remains poorly understood in clinical research and practice. To better understand resistant cancer cell heterogeneity, we isolated a novel riboflavin + NOTCH1 + population from cisplatin-naïve and -resistant lung cancer cell lines and patient specimens with or without immunotherapy and chemotherapy. This population was also identified as SLC52A2 (one of the riboflavin transporters) + NOTCH1 + cells in single-cell RNA sequencing (scRNA-seq) data derived from advanced lung tumors before therapy. Despite its therapy-naïve origin, the population, designated as stably resistant cancer cells (SRCC), exhibited the epithelial state, innate and stable resistance to therapy (chemotherapy, targeted therapy and immunotherapy), cell dormancy, elevated reactive oxygen species (ROS), and anti-apoptotic and anti-ferroptotic survival. These cellular and molecular characteristics distinguished SRCC from other resistant populations, including cancer stem-like cells (CSC), epithelial-mesenchymal transition (EMT) cells, and drug-tolerant persisters (DTP). The non-canonical NOTCH1 pathway, but not the inactivated canonical NOTCH1 pathway, played a critical role in the resistance of SRCC. Specifically, it modulates cell cycle, iron metabolism, EMT, and ferroptosis vulnerability in SRCC at the transcriptional level. It also controls the initiation of ferroptosis in lysosomes via a posttranslational NOTCH1-AKT-BAX axis. Inhibition of the non-canonical NOTCH1 pathway re-sensitizes these dormant and resistant cells to cisplatin-induced cell death in vitro and in vivo, including ferroptosis, apoptosis, and necroptosis. Our study contributes to a deeper understanding of cancer resistance and promotes the development of more effective therapeutic strategies against resistant cancer cells.
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BIOLOGICAL PROCEDURES ONLINE
·
2022
·Vol. 24
·期 1
·1-16
·
IF 7.717
Mei Jie,Cai Yun,Xu Rui,Yu Xinqian,Han Xu,Weng Miaomiao,Chen Lingyan,Ma Tao,Gao Tianshu,Gao Fei,Xia Tiansong,Zhu Yichao,Zhang Yan
Background Angiotensin-converting enzyme 2 (ACE2) is known as a tumor suppressor and lowly expressed in most cancers. The expression pattern and role of ACE2 in breast cancer (BC) have not been deeply elucidated. Methods A systematic pan-cancer analysis was conducted to assess the expression pattern and immunological role of ACE2 based on RNA-sequencing (RNA-seq) data downloaded from The Cancer Genome Atlas (TCGA). The correlation of ACE2 expression and immunological characteristics in the BC tumor microenvironment (TME) was evaluated. The role of ACE2 in predicting the response to therapeutic options was estimated. Moreover, the pharmacodynamic effect of angiotensin-(1–7) (Ang-1–7), the product of ACE2, on chemotherapy and immunotherapy was evaluated on the BALB/c mouse BC model. In addition, the plasma samples from BC patients receiving neoadjuvant chemotherapy were collected and subjected to the correlation analysis of the expression level of Ang-1–7 and the response to neoadjuvant chemotherapy. Results ACE2 was lowly expressed in BC tissues compared with that in adjacent tissues. Interestingly, ACE2 was shown the highest correlation with immunomodulators, tumor-infiltrating immune cells (TIICs), cancer immunity cycles, immune checkpoints, and tumor mutation burden (TMB) in BC. In addition, a high level of ACE2 indicated a low response to endocrine therapy and a high response to chemotherapy, anti-ERBB therapy, antiangiogenic therapy and immunotherapy. In the mouse model, Ang-1–7 sensitized mouse BC to the chemotherapy and anti-PD-1 immunotherapy, which revealed its significant anti-tumor effect. Moreover, a high plasma level of Ang-1–7 was associated with a better response to neoadjuvant chemotherapy. Conclusions ACE2 identifies immuno-hot tumors in BC, and its enzymatic product Ang-1–7 sensitizes BC to the chemotherapy and immunotherapy by remodeling the TME.
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Science China-Chemistry
·
2021
·Vol. 64
·期 10
·1796-1810
·
IF 9.445
Wu Cheng-Guang,Liang Jing-Lan,Wang Xiang,Zhou Xiaoyan,Cai Xiang,Xu Jun,Wang Meng,Wang Wen-Bo,Ma Dong,Xue Wei
The limited intratumoral perfusion of nitric oxide (NO)-carrying nanoparticles into solid tumors caused by the inherent biological barriers in vivo greatly attenuates their generated efficacy. Herein, through entrapping heat-sensitive NO donors (BNN6) on mesoporous polydopamine nanoparticles (M-PDA) and subsequently enveloping with red blood cells membranes, a heat-responsive biomimetic theranostic nanoerythrocyte (M/B@R) is developed to boost NO-based cancer therapy. The reserved intact structure of red blood cells membranes (RBCm) endows M/B@R with superior biosafety and stealth properties for prolonged circulation time and subsequent enhanced tumor accumulation. Once internalized in tumors and excited by near-infrared light (NIR, 808 nm) irradiation, M/B@R can not only yield plenty of heat for photothermal therapy (PTT) but also achieve the overproduction of NO for highly-efficient NO gas therapy due to its high loading capacity and NIR-absorbing property of M-PDA. The generated NO further ensures the formation of ONOO − which possesses remarkable toxicity to tumor as well as alleviating tumor hypoxia. It is found that M/B@R with NIR as the excitation source can significantly induce synthetic lethality to tumors via the hyperthermia, DNA damage and the ease of tumor hypoxia. Simultaneously, M/B@R also exhibits the potential for bimodal fluorescence and photothermal imaging. The RBCm-camouflaged NO delivery nanoplatform with bimodal imaging capability in this work may provide a new combinatorial paradigm to induce PTT/NO for cancer theranostic applications.
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EUROPEAN JOURNAL OF MEDICAL RESEARCH
·
2025
·Vol. 30
·期 1
·1275
·
IF 3.4
Xu Long,Zhao Yuanyuan,Song Shuxi,Liu Junling,Li Jingyu,Zheng Zhendong
Background Lung adenocarcinoma (LUAD) is a major cause of cancer-related morbidity and mortality globally, with challenges in prognosis and treatment due to its complex pathogenesis and heterogeneous tumor microenvironment (TME). Neutrophil extracellular traps (NETs) and oxidative stress play critical roles in tumor progression: NETs promote tumor cell adhesion, migration, and immune suppression, while oxidative stress induces DNA damage and activates pro-tumor signaling pathways. Moreover, oxidative stress is an important inducer of NETs, and their crosstalk shapes the LUAD immune microenvironment. However, systematic exploration of LUAD immunotherapeutic response prediction based on NETs and oxidative stress-related genes remains lacking. Methods The gene set related to oxidative stress was obtained from MSigDB. The gene set related to NETs was sourced from relevant literature. Transcriptomic and clinical data were integrated from The Cancer Genome Atlas (TCGA)-LUAD (training set) and GSE31210 (validation set). Weighted Gene Co-Expression Network Analysis (WGCNA) was employed to screen gene modules and characteristic scores related to NETs and oxidative stress signatures. Differentially expressed genes (DEGs) were screened, and prognostic model was established using univariate and LASSO Cox regression. Immune infiltration was analyzed using ESTIMATE algorithm, MCP-counter and ssGSEA methods. And we developed a nomogram incorporating clinicopathological features and RiskScore model, and performed drug sensitivity analysis. Finally, the biological role of CPS1 in lung cancer cells was investigated through CCK-8, wound-healing, and Transwell experiments. Results 22 co-expression modules were screened, among which the brown module showed significant correlations with NETs and oxidative stress signature scores. This module was intersected with DEGs, yielding 624 overlapping genes implicated in immune-relevant pathways (like leukocyte differentiation, neutrophil activation involved in immune response). A prognostic model was established utilizing 8 key genes ( ADGRE3 , ARHGEF3 , CD79A , CLEC7A , CPS1 , EPHB2 , LARGE2 , and OAS3 ). In the TCGA database, the model demonstrated robust prognostic discrimination (area under the curve (AUC) > 0.6), with high-risk patients exhibiting shorter overall survival (OS) ( p < 0.05). Its stability was validated in GSE31210 (AUC > 0.6). The RiskScore showed negative correlations with immune infiltration (like T cells, CD8 T cells, and natural killer cells) as well as immune/stromal scores. A nomogram model combining RiskScore with N staging was developed and validated, demonstrating strong predictive accuracy through calibration and decision curve analyses. High-risk patients were more sensitive to drugs like BI-2536, BMS-509744, and Pyrimethamine. Finally, in vitro tests showed that CPS1 knockdown markedly decreased the viability, migration, and invasion of lung cancer cells. Conclusion The constructed prognostic model by NETs and oxidative stress-relevant genes effectively predicts LUAD prognosis, correlates with immune microenvironment characteristics, and guides drug sensitivity, providing novel insights for LUAD prognostic assessment and personalized therapy.
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JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
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2022
·Vol. 78
·期 4
·777-791
·
IF 5.08
Li Ling,Bai Yu,Du Runyu,Tang Lei,Li Ling
Gestational diabetes mellitus (GDM) is a common pregnancy complication with a high incidence in women. Orphan nuclear receptor NUR77 is involved in regulating glucose metabolism. However, its role in GDM has not been fully elucidated yet. In this study, an animal model of GDM was established by feeding mice with a high-fat diet (HFD) before and during pregnancy. NUR77 expression was abnormally upregulated in placenta tissues of GDM mice. We performed gain- and loss-of-function studies of NUR77 in HTR-8/SVneo cells. Cells were incubated with 1 × 10 −6 M insulin for 48 h to induce insulin resistance (IR). The expression of NUR77 was downregulated in HTR-8/SVneo cells following IR induction. Overexpression of NUR77 promoted cell proliferation, migration, and invasion. Notably, NUR77 promoted glucose uptake and enhanced insulin sensitivity in vitro. NUR77 increased the ratio of p-insulin receptor β (IRβ) Tyr1361 /IRβ, p-insulin receptor substrate (IRS)-1 Tyr612 /IRS-1, p-Akt/Akt and decreased p-IRS-1 Ser307 /IRS-1, as well as lowered the expression of glucose transport protein type 1 (GLUT1) and elevated GLUT4. These results suggest the involvement of IRβ/IRS/Akt/GLUT4 signaling activation in the regulatory effects of NUR77 on IR in HTR-8/SVneo cells. Silencing of NUR77 displayed opposite effects. Besides, NUR77 enhanced the expression of autophagy-related protein Beclin 1 and the ratio of LC3II/LC3I. Further study demonstrated that the inhibitory effect of NUR77 on IR was partially attributed to the activation of autophagy. Therefore, we demonstrate that NUR77 enhances insulin sensitivity in HTR-8/SVneo cells likely through activating IRβ/IRS/Akt/GLUT4 pathway and regulating autophagy.
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JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
·
2019
·Vol. 38
·期 1
·1-12
·
IF 5.646
Shi Weidong,Zhang Chenyue,Ning Zhouyu,Hua Yongqiang,Li Ye,Chen Lianyu,Liu Luming,Chen Zhen,Meng Zhiqiang
Background Long non-coding RNA LINC00346 has been recently suggested as a prognostic marker in pancreatic cancer. However, its biological function in pancreatic cancer has not yet been determined. In this study, we attempted to ascertain the role of LINC00346 in regulating the aggressiveness of pancreatic cancer.Methods The effects of overexpression and knockdown of LINC00346 on the proliferation, cell cycle progression, apoptosis, and gemcitabine resistance were investigated. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were performed to search for potential microRNAs (miRs) that can interact with LINC00346.Results Overexpression of LINC00346 significantly enhanced the proliferation, colony formation, and tumorigenesis of pancreatic cancer cells. Conversely, knockdown of LINC00346 suppressed pancreatic cancer cell proliferation and caused a cell-cycle arrest at the G2/M-phase. Depletion of LINC00346 also enhanced gemcitabine sensitivity in pancreatic cancer cells both in vitro and in vivo. Mechanistic investigation revealed that LINC00346 acted as a sponge for miR-188-3p and blocked the repression of BRD4 by miR-188-3p in pancreatic cancer cells. Clinical evidence indicated a negative correlation between LINC00346 and miR-188-3p in pancreatic cancer specimens. Rescue experiments showed that LINC00346 attenuated the growth-suppressing and chemosensitizing effects of miR-188-3p on pancreatic cancer cells. In addition, silencing of BRD4 significantly inhibited LINC00346-induced pancreatic cancer cell proliferation and colony formation.Conclusion sLINC00346 shows the ability to promote pancreatic cancer growth and gemcitabine resistance, which is in part mediated by antagonization of miR-188-3p and induction of BRD4. Targeting LINC00346 may improve gemcitabine-based therapeutic efficacy.
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Microbiome
·
2023
·Vol. 11
·期 1
·1-23
·
IF 15.5
Hu Jun,Chen Jianwei,Xu Xiaojian,Hou Qiliang,Ren Jing,Yan Xianghua
Background The intestinal epithelial barrier confers protection against the intestinal invasion by pathogens and exposure to food antigens and toxins. Growing studies have linked the gut microbiota to the intestinal epithelial barrier function. The mining of the gut microbes that facilitate the function of intestinal epithelial barrier is urgently needed.Results Here, we studied a landscape of the gut microbiome of seven pig breeds using metagenomics and 16S rDNA gene amplicon sequencing. The results indicated an obvious difference in the gut microbiome between Congjiang miniature (CM) pigs (a native Chinese breed) and commercial Duroc × [Landrace × Yorkshire] (DLY) pigs. CM finishing pigs had stronger intestinal epithelial barrier function than the DLY finishing pigs. Fecal microbiota transplantation from CM and DLY finishing pigs to germ-free (GF) mice transferred the intestinal epithelial barrier characteristics. By comparing the gut microbiome of the recipient GF mice, we identified and validated Bacteroides fragilis as a microbial species that contributes to the intestinal epithelial barrier. B. fragilis-derived 3-phenylpropionic acid metabolite had an important function on the enhancement of intestinal epithelial barrier. Furthermore, 3-phenylpropionic acid facilitated the intestinal epithelial barrier by activating aryl hydrocarbon receptor (AhR) signaling.Conclusion sThese findings suggest that manipulation of B. fragilis and 3-phenylpropionic acid is a promising strategy for improving intestinal epithelial barrier.
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ANALYTICAL AND BIOANALYTICAL CHEMISTRY
·
2020
·Vol. 413
·期 4
·1073-1080
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IF 3.637
Chen Ye,Li Bin,Lyu Peng,Kwok Hang Fai,Ge Lilin,Wu Qinan
Phenylboronic acid-functionalized nanometer-sized CaCO 3 particles (PBA-CaCO 3 ) were designed to determine the carcinoembryonic antigen (CEA) glycoprotein with a portable Ca 2+ ion-selective electrode (Ca-ISE) through a typical boronate ester bond. CaCO 3 nanospheres were conjugated to 3-aminophenylboronic acid by amine-epoxy reaction, whereas target CEA was captured into the aptasensing interface by the immobilized thiolated aptamer on gold substrate. Upon PBA-CaCO 3 introduction, 3-aminophenylboronic acid labeled to CaCO 3 microsphere specifically recognized with CEA glycoprotein based on sugar-boronic acid interaction to form a sandwiched complex. The carried CaCO 3 was dissolved under acidic conditions to release Ca 2+ ion with a portable Ca-ISE readout. Thanks to the specific boronate ester bond between PBA and 1,2-diols, the synthesized PBA-CaCO 3 exhibited good conjugation properties for CEA glycoprotein. Under optimum conditions, Ca-ISE-based aptasensing platform exhibited good electrode potential response for evaluation of target CEA, and allowed detection of CEA at a concentration as low as 7.3 pg mL −1 . Importantly, Ca-ISE-based aptasensing system is readily extended to detect other disease-related glycoproteins by controlling the corresponding aptamer.
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