SENSORS AND ACTUATORS B-CHEMICAL
·
2024
·
IF 8
Yanmei Lu,Jiayue Liu,Yufang Hu,Wenjun Dong,Caizhao Cheng,Zhihe Qing,Shun Zhang
Visual detection of histone acetylation in cells is highly desirable for medical diagnostics, particularly in cancer. Currently, a single substrate-indicated multi-mode visual platform has been developed for detecting the activity of acetyltransferase (KAT Tip60) in circulating tumor cells (CTCs) of esophageal cancer. o-Phenylenediamine (OPD) serves as a single indicator in our constructed multi-mode analytical method, where the introduction of Cu(II) stimulates a change in fluorescent/UV–vis signals and colors. However, coenzyme A (CoA), a byproduct of the acetylation process, effectively prevents the interaction between Cu(II) and OPD, and this competitive reaction is aptly associated with the KAT Tip60-domonicated acetylation process. Good linear relationships are observed between the optical signals in the multi-mode method and the logarithms of the Tip60 concentration, with detection limits of 0.0045 ng/mL (fluorescence) and 0.058 ng/mL (UV–vis), respectively, calculated as 3σ/slope. To meet the needs of smart/precision medicine, a smartphone-based visualization approach tailored to the red-green-blue (RGB) color space is developed via Cu(II)-OPD redox catalysis. This approach is successfully employed for the analysis of Tip60-indicated acetylation in CTCs of esophageal cancer. This study establishes an important foundation for advancing RGB color-based smartphone modes for actual analyses, and integrating another catalytic unit based on the single OPD substrate presents a viable strategy for analyzing other biomarkers in cancer-targeted clinical applications.
研究领域:
医学诊断
·
癌症研究
·
生物化学
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF PROTEOME RESEARCH
·
2024
·
IF 3.8
Jijuan Zhou,Dianlong Ge,Yajing Chu,Yue Liu,Yan Lu,Yannan Chu
Detection of exhaled volatile organic compounds (VOCs) is promising for noninvasive screening of esophageal cancer (EC). Cellular VOC analysis can be used to investigate potential biomarkers. Considering the crucial role of methionine (Met) during cancer development, exploring associated abnormal metabolic phenotypes becomes imperative. In this work, we employed headspace solid-phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC-MS) to investigate the volatile metabolic profiles of EC cells (KYSE150) and normal esophageal epithelial cells (HEECs) under a Met regulation strategy. Using untargeted approaches, we analyzed the metabolic VOCs of the two cell types and explored the differential VOCs between them. Subsequently, we utilized targeted approaches to analyze the differential VOCs in both cell types under gradient Met culture conditions. The results revealed that there were five/six differential VOCs between cells under Met-containing/Met-free culture conditions. And the difference in levels of two characteristic VOCs (1-butanol and ethyl 2-methylbutyrate) between the two cell types intensified with the increase of the Met concentration. Notably, this is the first report on VOC analysis of EC cells and the first to consider the effect of Met on volatile metabolic profiles. The present work indicates that EC cells can be distinguished through VOCs induced by Met regulation, which holds promise for providing novel insights into diagnostic strategies.
研究领域:
肿瘤学
·
代谢组学
·
医学检测
✓ 已验证
DOI
PubMed
高影响因子
OPTICS COMMUNICATIONS
·
2023
·
IF 2.4
Kaixin Ge,Renhao Ni,Pan Tao,Xiangfen Zhao,Yang Luo,Yabin Zhu,Baoan Song,Wei Zhang,Shixun Dai,Ning Zhang,Tiefeng Xu,Peiqing Zhang
The early detection of esophageal cancer is crucial for enhancing patient survival. Surface-enhanced Raman scattering (SERS), renowned for its precise detection capabilities of low-concentration molecules and organisms, holds immense promise for early diagnosis. However, the use of silver nanoparticles to enhance the Raman signal can disrupt the detection process. To address this problem in this study, we synthesized polyethylene glycol (PEG)-coated silver nanocubes (PEG-AgNCs) as stable, label-free, and low-toxicity nanoprobes for detecting esophageal cancer. AgNCs with sharp corners and edges are selected as the SERS substrate to increase the strength of the Raman signal. To minimize the toxicity of AgNCs, the surface is coated with PEG, which exhibits outstanding biocompatibility. The SERS effectiveness of PEG-AgNCs was evaluated using 4-mercaptobenzoic acid as a Raman probe molecule, and the toxicity of PEG-AgNCs at different concentrations was investigated using human keratinocytes (HaCaT) and human esophageal carcinoma cells (TE-1). Results showed that PEG-AgNCs can effectively reduce the toxicity of AgNCs while maintaining a strong SERS signal. Remarkable differences in Raman spectra were observed between HaCat and TE-1 cells within the spectral range of 588–768 cm −1 , indicating the potential of PEG-AgNCs in the early detection of esophageal cancer using Raman detection. Our study highlights the potential of developing low-toxicity SERS biosensors for biological and chemical analyses.
✓ 已验证
产品关联
DOI
高影响因子
ANTIOXIDANTS & REDOX SIGNALING
·
2026
·
IF 6.1
Ze Wang,Kejie Chang,Ke Zhang,Pei Wang,Guangjian Bai,Zhenhua Wang,Jian Xiao,Xin Tong,Jun Zhao
Aims:Esophageal squamous cell carcinoma (ESCC) is among the most lethal malignancies worldwide, with a five-year survival rate below 20%. Ferroptosis—a regulated form of cell death driven by iron-dependent lipid peroxidation—has emerged as a promising therapeutic strategy, yet its regulation in ESCC remains poorly understood. We investigated the role of tripartite motif-containing 31 (TRIM31), an E3 ubiquitin ligase, in ESCC progression and ferroptosis.Results:TRIM31 expression was significantly elevated in ESCC tissues compared with normal esophageal tissues (The Cancer Genome Atlas and Genotype-Tissue Expression datasets; p < 0.001) and correlated with advanced Tumor, Node, and Metastasis (TNM) stage (p = 0.004), lymph node metastasis (p = 0.024), and poor overall survival (p = 0.0027). Functional assays revealed that TRIM31 knockdown reduced ESCC cell proliferation, impaired colony formation, and suppressed migration (p < 0.01). In vivo, TRIM31 silencing decreased xenograft tumor volume by over 70% and Ki-67 expression by 73%. Mechanistically, TRIM31 directly interacted with VDAC1 via its coiled-coil domain, promoting VDAC1 ubiquitination and proteasomal degradation. This interaction inhibited ferroptosis, as evidenced by increased lipid reactive oxygen species, elevated intracellular Fe2+ levels, and mitochondrial damage upon TRIM31 knockdown. Conversely, TRIM31 overexpression attenuated ferroptosis induced by RSL3. We further identified hepatocyte nuclear factor 4 alpha as a transcriptional activator of TRIM31, binding to its promoter region. Importantly, TRIM31 knockdown synergized with the ferroptosis inducer imidazole ketone erastin, achieving a 90% reduction in tumor growth without significant toxicity.Conclusion:TRIM31 promotes ESCC progression by degrading VDAC1 and suppressing ferroptosis. Targeting TRIM31 enhances ferroptosis-based therapy and represents a novel, clinically actionable strategy for ESCC treatment. Antioxid. Redox Signal. 00, 000–000.
✓ 已验证
DOI
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2022
·
IF 7.419
Guodong Ren,ZiCheng Wang,Yafei Tian,Jinyao Li,Yingyu Ma,Liang Zhou,Chengwu Zhang,Lixia Guo,Haipeng Diao,Lihong Li,Li Lu,Sufang Ma,Zhifang Wu,Lili Yan,Wen Liu
As the sixth leading cause of cancer death, esophageal cancer is threatening the life of people worldwide. Traditional treatments, such as surgery, chemotherapy, radiotherapy, are facing always augmented challenges including invasion, multidrug resistance (MDR), off-target toxicity. Chemo & Photodynamic synergistic therapy represents one promising strategy for improved treatment efficiency. But it is still hindered by the lack of tumor targeting, deleterious side effects, and unfavorable microenvironment for photodynamic therapy (PDT). To overcome those obstacles, one theranostic nano-assambly drug, GCDs-Ce6/Pt-EGF, was designed and fabricated. Green fluorescence carbon dots (GCDs) with the excellent optical properties, modifiability and low toxicity were prepared as drug carrier. Epidermal growth factor (EGF) was conjugated to the nano-assembly to realize tumor specific targeting. Chlorin e6 (Ce6) in the presence of laser irradiation achieved PDT by generating proapoptosis reactive oxygen species (ROS). Moreover, Ce6 incorporated into GCDs endowed the nano-assambly imaging ability and facilitate image-guided therapy. Pt(IV), cisplatin prodrug, in the nano-assambly depleted the glutathione (GSH) of tumor microenvironment when it was reduced to cytotoxicity Pt(II). Compared with single treatment, GCDs-Ce6/Pt-EGF exhibited enhanced tumor cell killing capacity and better biosafety in vitro and in vivo , especially for EGFR bearing tumor. It paved ways for developing novel theranostic agent to be potentially applied in clinic.
研究领域:
癌症治疗
·
纳米技术
·
药物科学
·
生物医学工程
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2024
·
IF 4.4
Gaobing Ye,Shiyao Luo,Hajra Zafar,Honglei Ge,Binbin Liu,Nan Wang,Yu Jin,Miao Wang,Xu Chen,Xiaoming Ye
Esophageal cancer is one of the most common cancers in the world, ranking sixth in cancer-related mortality. Doxorubicin (DOX), as a classic broad-spectrum, non-specific small-molecular anti-tumor drug, has achieved widespread use, including in the treatment of esophageal cancer. However, due to its strong cardiotoxicity, poor tumor-targeting ability, and short half-life, the clinical application of DOX has been greatly limited. In this research, we designed and successfully synthesized a peptide sequence IEIIIK (IEK for short) with excellent pH responsiveness. Under physiological conditions (pH 7.4), the peptide can encapsulate DOX and self-assemble into a stable hydrogel (DOX-IEK) through hydrophobic and electrostatic interactions. After being injected into the acidic tumor microenvironment, the protonation degree of alkaline amino acid lysine increased and the negative charge of glutamate decreased, directly leading to enhanced electrostatic repulsion and subsequent hydrogel dissociation. Released DOX can accumulate in tumor tissue and achieve anti-tumor efficacy. More importantly, the hydrogel can act as a drug reservoir for sustained drug release, improving the drug targeting ability, prolonging the duration of drug administration to compensate for the short half-life of DOX, and reducing systemic toxicity. Ideal anti-tumor efficacy has been achieved in both the in vitro and in vivo experiments.
研究领域:
生物医学工程
·
药剂学
·
肿瘤学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
International Journal of Nanomedicine
·
2026
·
IF 8.7
Jiahao Huang,Shufeng Liang,Min Zhang,Yue Zheng,Chunyan Wang,Xin Tian,Bin Yang
Purpose Iodine-125 (125I) brachytherapy delivers continuous low-dose γ-irradiation for advanced esophageal cancer, but its efficacy is constrained by intrinsic tumor radioresistance and by the risk of normal-tissue injury arising from shedding of the radionuclide from the tumor site. This study aimed to develop a multifunctional nanoplatform coupling 125I delivery with photothermal-enhanced radiosensitization for synergistic therapy.Methods A polymeric peptide-functionalized graphdiyne (GDY) nanoplatform (GDY-PEG-PTyr) was constructed by conjugating an amphiphilic PEG-PTyr copolymer (prepared by ring-opening polymerization of tyrosine N-carboxyanhydride) onto GDY nanosheets, followed by 125I labeling via chloramine-T oxidation. The nanocomposite was characterized by TEM, XRD, Raman, XPS, FTIR, and thermogravimetric analysis, and its photothermal behavior was evaluated under 808 nm near-infrared (NIR) irradiation. Therapeutic efficacy and underlying mechanisms were assessed in KYSE-150 esophageal carcinoma cells and in tumor-bearing mice using cell viability, reactive oxygen species (ROS), γ-H2AX, live/dead, and histological assays.Results GDY-PEG-PTyr exhibited a two-dimensional sheet-like morphology, a high radiolabeling yield (~95%), and radiochemical stability above 80% over 72 h, and it reached mild hyperthermia (42–45 °C) with reproducible photothermal output over repeated heating–cooling cycles. In vitro, the combined GDY-PEG-PTyr-125I + NIR treatment reduced cell viability to 16.15%, far below that of either modality alone, while generating the strongest intracellular ROS signal, the most γ-H2AX foci, and pronounced upregulation of BAX and Caspase-3. In vivo, this combination produced near-complete tumor regression, with complete tumor elimination in three of five mice, and induced no detectable systemic toxicity.Conclusion The GDY-PEG-PTyr-125I nanoplatform integrates radionuclide brachytherapy with photothermal therapy, in which localized hyperthermia amplifies radionuclide-induced oxidative stress and DNA double-strand breaks to drive apoptosis, offering a promising nanomedicine strategy for overcoming radioresistance in esophageal cancer.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
·
2020
·Vol. 52
·期 8
·842-852
·
IF 2.836
Zhang Liang,Wang Xin,Liu Xin,Lv Mingyue,Shen Erdong,Zhu Guolian,Sun Zhe
Esophageal cancer (EC) is one of the most common aggressive malignant diseases worldwide. miR-28-5p plays important regulatory roles in many cancers including human EC. However, the molecular mechanism and potential role of miR-28-5p in EC remain uncertain. In this study, qRT-PCR and western blot analysis revealed that miR-28-5p expression was up-regulated and metastasis suppressor-1 (MTSS1) was down-regulated in EC tissues relative to matched para-cancer tissues. Cell counting kit-8 (CCK-8) assay demonstrated that miR-28-5p mimics increased cell viability, and miR-28-5p inhibitor decreased it. Flow cytometry (FCM) assay indicated that miR-28-5p mimics promoted cell cycle entry, while miR-28-5p inhibitor reduced it and induced cell apoptosis. Moreover, miR-28-5p mimics up-regulated the expressions of cyclin A, cyclin dependent kinase 2 (CDK2), cyclin D1, and cyclin E but down-regulated the expressions of cleaved caspase-3 and cleaved caspase-9, which was abolished by miR-28-5p inhibitor. Furthermore, luciferase reporter assay verified that miR-28-5p directly targeted MTSS1 3′UTR and down-regulated its expression. MTSS1 overexpression in TE-1 cells inhibited cell proliferation and promoted apoptosis induced by miR-28-5p mimics, whereas silencing of MTSS1 reversed cell progression induced by miR-28-5p inhibitor. We also demonstrated that miR-28-5p could promote esophageal tumor formation in vivo. Hematoxylin–eosin staining, immunohistochemistry, and TUNEL assays confirmed that miR-28-5p antagomir inhibited cell growth and accelerated apoptosis. Our results suggest that miR-28-5p may induce cell proliferation and suppress apoptosis to promote EC tumor formation via decreasing MTSS1 expression. Thus, miR-28-5p may be a potential target for human EC therapy.
研究领域:
肿瘤学
·
分子生物学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
·
2026
·
IF 8.3
Shijin Zhou,Nan Ma,Baolin Huang,Qian Yang,Jinming Kong,Xueji Zhang
An ultrasensitive electrochemical biosensor has been developed for the detection of miRNA-320b, an exosomal RNA biomarker associated with lymph node metastasis in esophageal squamous cell carcinoma (ESCC). The platform employs a molybdenum-catalyzed atom transfer radical polymerization (Mo-ATRP) signal amplification strategy, eliminating the need for enzymatic or thermal amplification and enabling cost-effective, early-stage cancer diagnostics. A thiolated peptide nucleic acid (PNA) probe is immobilized on a gold electrode to specifically capture miRNA-320b. Upon hybridization, a sodium molybdate (Na 2 MoO 4 )-catalyzed ATRP reaction, initiated by tetrahydrocurcumin (THC), drives the in situ polymerization of 4-methacryloyloxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) monomers, forming redox-active polymer brushes directly on the electrode surface. The electrochemical response is exclusively derived from the surface-confined poly(TEMPO) layer, which forms only upon successful target recognition, ensuring high signal-to-noise performance. The biosensor achieves a detection limit of 0.417 fM with a linear range spanning 1 × 10 −15 to 1 × 10 −10 M ( R 2 = 0.992) and demonstrates excellent selectivity and robustness in complex biological matrices. Its resistance to common interferents and consistent performance under real-sample conditions underscore its suitability for clinical translation. This Mo-ATRP-based highly sensitive approach provides a promising foundation for non-invasive liquid biopsy and early detection of aggressive cancers such as ESCC.
✓ 已验证
DOI
高影响因子
RARE METALS
·
2026
·Vol. 45
·期 8
·e70441
·
IF 12.1
Mengya Li,Ruimei Jin,Shengxi Zhou,Jingan Li,Kun Zhang
en This link goes to a English section zh This link goes to a Chinese section Esophageal cancer is the seventh leading cause of cancer death, and the energy depletion in cancer cells can be achieved through synergistic therapy. The integration of sonodynamic therapy and chemotherapy offers a promising comprehensive treatment strategy for esophageal cancer. However, a significant challenge lies in the efficient delivery of sound sensitizers and therapeutic agents. Herein, we present an energy-depleting biomimetic Zeolitic imidazolate framework-8 (ZIF-8) nanoparticle with high encapsulation efficiencies for the sonosensitizer Indocyanine green (ICG) and the chemotherapeutic agent Doxorubicin (DOX). By coating the nanoplatform with esophageal cancer cell membranes, we achieve enhanced homologous targeting to esophageal cancer cells, termed ICG/DOX/ZIF-8@M. In vitro and in vivo experiments demonstrated significant inhibition of tumor growth when treated with ICG/DOX/ZIF-8@M and ultrasonic stimulation. Single-cell RNA sequencing and mechanistic studies further elucidated the downregulation of energy metabolism-related pathways, including glutamine metabolism and glycolysis, which contribute to the enhanced efficacy of the combined therapy. Targeting and energy-depleting biomimetic ICG DOX/ZIF-8@M nanoparticles represent a promising strategy for esophageal cancer therapy. 摘要 en This link goes to a English section zh This link goes to a Chinese section 声动力疗法与化疗协同治疗策略可显著实现肿瘤能量耗竭, 抑制肿瘤生长, 是治疗食管鳞癌的一种前景广阔的策略。然而, 如何实现声敏剂和和化疗药物的高效递送仍然是一个重大挑战。为此, 我们开发了一种能量耗竭型仿生ZIF-8纳米颗粒(ICG/DOX/ZIF-8@M), 对声敏剂吲哚菁绿和化疗药物多柔比星具有极高的包封率, 采用食管癌细胞膜包覆可以通过同源靶向作用实现药物高效递送。体外和体内实验结果表明, ICG/DOX/ZIF-8@M联合超声处理显著抑制肿瘤生长。单细胞RNA测序与分子水平研究表明, ICG/DOX/ZIF-8@M显著下调谷氨酰胺代谢和糖酵解等能量代谢相关通路, 实现肿瘤能量耗竭。综上, 靶向能量耗竭型仿生ICG/DOX/ZIF-8@M纳米颗粒为食管癌治疗提供了一种富有前景的治疗策略。
✓ 已验证
产品关联
DOI
高影响因子
Scientific Reports
·
2026
·
IF 4.9
Zhao Chao,Xia Yuchen,Shi Qingtong,Gu Yun,Zhang Long,Dong Ruijun,Zhang Yuxuan,Han Sifan,Jiang Yimeng,Xiong Wen,Guo Hong,Wang Bing,Xia Junpeng,Wang Qianqian,Zhang Hu,Bao Yafei
Although nitrosamines are known as potent carcinogenic contaminants with multisystem toxicity, the metabolic mechanisms driving esophageal carcinogenesis under multi-nitrosamine co-exposure remain poorly understood. This molecular epidemiological study sought to identify dynamic metabolic signatures mediating nitrosamine-associated esophageal squamous cell carcinoma (ESCC) risk. We quantified urinary levels of nine nitrosamines in participants across esophageal lesion stages (RE/BCH, DYS, ESCC) and employed UPLC-MS/MS metabolomics to investigate exposure-response relationships and mediation effects of key metabolites. Distinct stage-specific nitrosamine profiles were observed. Sphingolipid metabolism emerged as a critical pathway in ESCC pathogenesis: DH-SPH, DH-S1P, and S1P were positively associated with increased risk, while SPH and the SPH/S1P ratio demonstrated protective effects. Mediation analysis revealed metabolite-specific pathways, with DH-S1P acting as a shared mediator in NDphA-, NMEA-, and NPIP-induced ESCC pathways, and S1P mediating NMEA-associated progression from RE/BCH to ESCC. Sensitivity analyses indicated differential robustness across pathways. E-value assessment revealed that NDphA-related pathways exhibited high resistance to unmeasured confounding (E-value > 2). Critical ρ analysis indicated that DH-S1P-mediated pathways in ESCC exhibited high credibility (ρ thresholds ≈ 0.3), and SPH/S1P-mediated pathways yielded conservative effect estimates. ROC analysis with bootstrapping validation suggested the potential discriminative ability of sphingolipid metabolites: S1P showed promise in distinguishing across the disease spectrum, and a combined panel demonstrated improved performance for ESCC prediction and nitrosamine exposure discrimination in this study population. Collectively, these findings underscore sphingolipid dysregulation as a key associative mediator linking nitrosamine exposure to ESCC progression, and support their potential as candidate biomarkers for early screening and exposure monitoring in high-risk populations. However, due to the cross-sectional design and absence of external validation, these findings await confirmation in prospective and functional studies.
✓ 已验证
DOI
PubMed
高影响因子
Cancer Genetics
·
2025
·
IF 2.1
Yuan Wang,Xin Wan,Yutian Zhang,Jia Qi,Chao Li,Xiaonan Cui
Objective To explore the role of ESRRA in esophageal squamous cell carcinoma (ESCC) progression and evaluate the antitumor effects of hydroxygenkwanin (HGK), focusing on its interaction with ESRRA and the underlying molecular mechanisms. Methods Cell viability, apoptosis, invasion, and proliferation were assessed in EC109 and TE-1 cells treated with HGK using CCK-8, Hoechst staining, Transwell, and colony formation assays. ESRRA expression was analyzed via qPCR and Western blot. An ESCC mouse model was established, with treatment groups receiving HGK. Serum IL-10 and IL-12 levels were measured by ELISA; tumor growth and toxicity were evaluated by histology. EMT marker expression was analyzed by IHC and RT-qPCR. TCGA database analysis explored ESRRA-related pathways and its link to the tumor microenvironment and patient survival. Results HGK inhibited EC109 and TE-1 cell proliferation and migration, especially in EC109 cells, by downregulating ESRRA in a dose-dependent manner. In vivo, HGK reduced tumor growth with minimal toxicity, though high doses showed possible renal effects. IL-12 levels decreased, and EMT markers were altered. ESRRA was overexpressed in ESCC tissues and correlated with EMT-related genes. TCGA analysis confirmed ESRRA’s association with poor survival in ESCC patients. Conclusion HGK effectively suppresses ESCC with low toxicity, primarily by inhibiting ESRRA and blocking EMT, highlighting its therapeutic potential.
研究领域:
肿瘤学
·
分子生物学
·
药理学
·
转化医学
·
信号转导
✓ 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）