ANALYTICAL CHEMISTRY
·
2026
·Vol. 98
·期 28
·20936-20944
·
IF 7.3
Liu Ziyu,Xie Lingling,Yin Shuhang,Zhu Xiaohua,Liu Meiling,Zhang Youyu
Cellular signaling networks are orchestrated by complex
interactions
between gene expression and ion flux, yet tools for simultaneously
visualizing these events in living cells remain limited. Herein, we
report two orthogonal gold-nanoparticle-based DNA nanosensors that
enable simultaneous imaging of sodium/hydrogen exchanger 1 (NHE1)
mRNA and Na + dynamics in hepatocellular carcinoma cells.
The sensing mechanism relies on proximity-dependent fluorescence quenching.
For mRNA detection, Cy3-labeled reporter strands hybridize to DNA-functionalized
gold nanoparticles (AuNPs), holding the fluorophore close to the quenching
surface. Target binding triggers strand displacement, releasing Cy3,
and restoring emission. For Na + detection, a Cy5-labeled
substrate strand hybridizes with a Na + -specific DNAzyme
anchored on AuNPs. Na + activates the DNAzyme, cleaving
the substrate at a defined site and liberating the Cy5 fluorophore.
This dual-sensor system enables the quantitative monitoring of both
analytes in living cells. Using this platform, we directly visualize
that NHE1 mRNA downregulation suppresses intracellular Na + accumulation, establishing a regulatory link between gene expression
and ion homeostasis. Notably, mRNA-targeted hybridization inhibits
cancer-cell migration in a dose-dependent manner, revealing a potential
therapeutic mechanism. This approach provides a molecular tool for
decoding ion-based signaling networks in cancer biology.
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OPTICS AND LASER TECHNOLOGY
·
2026
·
IF 5.2
Like Li,Shunye Huang,Yi Li,Xiaoman Chen,Qiwei Li,Hui Tang,Xuqiang Wu,Yong Zhao
Due to its narrow treatment window, the vancomycin concentration in the patient’s body needs to be monitored regularly to guide dose optimization and ensure safety and efficacy. Here, we developed a fiber-optic surface plasmon resonance (SPR) vancomycin sensor based on gold nanoparticles (AuNPs)/multiwalled carbon nanotubes (MWCNTs)/DNA aptamer synergistic modification. AuNPs can effectively enhance the local electromagnetic field and plasmon resonance effects, while MWCNTs have a strong electronic conductivity and a high specific surface area. The synergistic effect of the two can achieve dual amplification of the SPR signal, thereby improving the sensitivity. Vancomycin aptamer can specifically capture vancomycin molecules and induce spatial conformational changes, thereby increasing the effective refractive index. Experimental results confirmed that within 30 μM–400 μM, the sensitivity of vancomycin detection is as high as 0.0527 nm/μM, and the detection limit is 18.11 μM. Moreover, the vancomycin sensor exhibits excellent stability and specificity. The vancomycin sensor is low-cost, easy to use, and has the potential to be applied for rapid and accurate determination of vancomycin in clinical settings.
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ANALYTICA CHIMICA ACTA
·
2026
·
IF 6.1
Ruo-Yao Cui,Yu-Chao Cao,Yi-Xuan Gu,Ling-Li Zhao,Xu-Yang Shen,Ying Liu,Ying-Lin Zhou,Xin-Xiang Zhang
Background G-quadruplexes (G4s) act as versatile scaffolds for biosensing, yet a generalizable strategy to systematically amplify the fluorescence of G-rich scaffold-bound molecular rotors remains lacking. Results Herein, we propose a G-run-length engineering strategy to enhance the “light-up” performance of fluorogenic ligands using Thioflavin T (ThT) as a model molecular rotor. Through rational design of a sequence library derived from EAD4 with variable G-run lengths (N = 2–6, where N denotes the number of consecutive guanines per G-tract), we show that increasing N progressively amplified ThT fluorescence by up to ∼1000-fold under metal-free conditions. Mechanistic investigations—including induced circular dichroism, thermal melting analysis, Job plots, isothermal titration calorimetry and hydroxylation kinetics—support that G-run extension increases ligand-accessible binding environments and shields bound ThT from the aqueous phase, thereby restricting intramolecular rotation and suppressing non-radiative decay. The enhanced shielding likely arises from strengthened terminal stacking and/or possible cavity-associated binding, although the present data do not define a single G4 topology or a unique microscopic binding mode. The G-run-length-dependent enhancement trend was further observed in derivative libraries based on different G-rich DNA scaffolds and with other molecular rotors, including Thiazole Orange and Auramine O, suggesting functional generalizability. By contrast, macrocyclic planar ligands such as hemin and N-Methyl Mesoporphyrin IX, which are dominated by terminal G-tetrad association rather than intramolecular rotation restriction, did not show the same trend. Significance These findings establish G-run-length engineering as a practical strategy for regulating G-rich scaffold–fluorophore interactions and provide mechanistic guidance for nucleic-acid-based fluorescence signal amplification.
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JOURNAL OF INORGANIC BIOCHEMISTRY
·
2026
·
IF 3.1
Zhijian Zhang,Zhongshan Zhou,Wujiu Jiang,Yuxing Tan
Four organotin acridine-9-carboxylate complexes ( C1 – C4 ) were successfully synthesized by the reaction of 9-acridinecarboxylic acid ( YCOOH ) with organotin precursors. The structures of these complexes were systematically characterized using elemental analysis, IR, NMR, X-ray single-crystal diffraction, X-ray powder diffraction and thermogravimetric analysis. Among them, the tributyltin complex C4 exhibited the most potent in vitro antiproliferative activity against HepG2, MCF-7, and NCI-H460 cancer cell lines, with IC 50 values as low as 0.08 μM against HepG2 cells. Mechanistic studies identified two functional pathways: (i) DNA intercalation, as evidenced by UV–Vis, fluorescence titrations, viscosity measurements, and molecular docking, which directly disrupts DNA architecture; and (ii) mitochondria-mediated apoptosis, characterized by collapse of mitochondrial membrane potential (Δ Ψ m ), cytochrome c (Cyt C) release, elevated ROS generation, upregulation of Bax and Cleaved-caspase-3, and downregulation of Bcl-2. Importantly, these two pathways act synergistically: DNA intercalation triggers early nuclear stress, which amplifies mitochondrial dysfunction and ROS burst, thereby lowering the apoptotic threshold and enhancing the overall cytotoxic efficacy. Collectively, the dual DNA-mitochondria targeting and their cooperative action establish acridine-based organotin complexes as promising anticancer candidates.
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ACS Omega
·
2026
·
IF 5.2
Ai Chen,Shuo Ma,Jiwei Wang,Yuming Yao,Gulinaizhaer Abudushalamu,Meiling Zhou,Dawen Chen,Yue Zheng,Chenyan Yuan,Chuankun Yang,Xun Gao,Chen Zhang,Guoqiu Wu
Norovirus is a major cause of acute gastroenteritis, yet rapid diagnostics that combine scalability, high analytical sensitivity, and minimal instrumentation remain limited. Here, we report an enzyme-free nucleic acid detection platform that integrates catalytic hairpin assembly (CHA) with lateral flow readout in two formats: a visual colloidal-gold strip (CHA-GICA) and a fluorescence strip (CHA-FICA). A conserved 23-nt sequence shared across norovirus GI and GII triggers CHA at 35 °C to generate biotin- and digoxin-labeled duplex products, which are captured on the test line via antidigoxin binding, while excess reporters are retained at the control line. The workflow requires 30 min total (15 min reaction and 15 min strip development). Under optimized conditions, CHA-GICA achieved a limit of detection of 10 pM, and CHA-FICA reached 100 fM, with strong discrimination against single-base substitutions and small insertion/deletion variants. Hairpin probes remained stable for at least 4 weeks at −20 °C and were suitable for short-term storage at 4 °C. In 55 clinical fecal specimens benchmarked against RT-qPCR (15 positive, 40 negative), CHA-GICA showed 73.3% sensitivity and 100% specificity (AUC = 0.853), while CHA-FICA improved sensitivity to 86.7% with 100% specificity (AUC = 0.988). This dual-format, enzyme-free CHA lateral flow platform enables rapid norovirus screening with flexible deployment, supporting instrument-free field testing by CHA-GICA and higher-sensitivity detection by CHA-FICA.
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ANALYTICAL CHEMISTRY
·
2026
·
IF 7.3
Yong Li,Xiangyu Chen,Ye Wang,Xiaowen Zhao,Jiansen Du,Chao Shi,Cuiping Ma
DNA methylation serves as a crucial biomarker for early cancer detection, holding great promise in liquid biopsy. However, its low abundance in plasma and interference from complex matrices pose significant challenges to clinical detection sensitivity. To this end, this study developed a novel direct enrichment platform based on methyl-binding domain (MBD) protein-functionalized magnetic nanoparticles (MBD@MNPs). Through systematic optimization, the methylated DNA (mDNA) capture efficiency of MBD@MNPs reached 86.6% with an elution efficiency of 44.9% in simulated systems, while bypassing the cumbersome step of total cell-free DNA (cfDNA) extraction and overcoming plasma matrix interference. In comparison, this strategy enhanced the sensitivity of methylation-specific PCR by 25-fold, with a detection limit as low as 0.04 ng/mL. Applied to plasma samples from patients with various tumors (including colorectal, lung, breast, cervical, liver, and gastric cancers), the technology significantly improved the detection rates up to 100% of tumor-specific methylation biomarkers, such as SDC2, SHOX2, RASSF1A, ZNF671, Septin9, and BMP3. Therefore, this study provides an efficient, universal and user-friendly enrichment and accurate detection of mDNA, laying a methodological foundation for early cancer screening and prognosis assessment.
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ANALYTICAL CHEMISTRY
·
2025
·
IF 6.7
Ruoyu Hu,Wei Wang,Hui Wang
Disclosing the stimuli-responsive dynamics of nanoliposomes and interdependence of interfaces is central for the transport and release of biomolecules in signal transduction and intracellular trafficking processes. Here, we utilized a noninvasive plasmonic imaging strategy for directly visualizing the phospholipid-molecule mobility and DNA-programmed combinatorial membrane fusion events down to the single nanoliposome level. Distinct intermediate states and thermodynamics during the transient interplay between a single nanoliposome and interfaces can be recognized until reaching the equilibrium stage. Spatial discrimination of a single nanoliposome regulated by external stimulus reveals stepwise diffusion kinetics attributed to the heterogeneous phospholipid-molecule collapse behavior. Furthermore, the real-time programmable fusion event induced by orthogonally hybridizing sets of membrane-anchored DNA molecules is captured for lipidic nanoreactors, which uncovers the specific dynamics and mechanism information. This imaging strategy shows potential in characterizing chemical engineered and functionalized nanoscale reactors and containers in biological systems.
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BIOSENSORS & BIOELECTRONICS
·
2025
·
IF 10.5
Wen Tian,Tao Liu,Xiaoying Niu,Po Li,Zhehuang Li,Songcheng Yu,Peng Zhang
DNA methylation serves as a critical epigenetic biomarker for early disease screening and clinical diagnostics, exemplified by the FDA-approved detection of methylated Septin9 gene in peripheral blood for colorectal cancer (CRC) screening. Conventional CRISPR/Cas12a-based detection systems rely on fluorophore-quencher-labeled ssDNA probes to transduce trans-cleavage activity into fluorescence signal, which yet suffers from limitations including complex probe synthesis, background noise induced by incomplete quenching and high cost. In this study, we developed a cascaded and label-free CRISPR/Cas12a system for Septin9 methylation detection using DNAzyme and split DAP-10. The method employed methylation-sensitive Aci I digestion to selectively hydrolyze non-methylated DNA, leaving methylated Septin9 DNA fragment intact to activate CRISPR/Cas12a system. Activated Cas12a triggered trans-cleavage of DNAzyme, a bifunctional molecule that acted as both trans-cleavage substrate of Cas12a and hydrolysis regulator of linker DNA that facilitated split DAP-10 reassembly to light-up Auramine O (AO) fluorescence proportionally to methylation levels. The assay achieved a linear range from 2 to 200 nM with a detection limit of 1.74 nM and robust performance in accuracy, precision, and selectivity. The proposed method was successfully applied in methylated Septin9 detection in cell lines, clinical tissues and blood samples, which indicated application potential for CRC screening.
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TOXICOLOGY LETTERS
·
2025
·
IF 2.9
Xulong Cai,Qiaolan Xu,Tongjin Yin,Xia Li,Yan Cheng,Xiangning Li,Chuangli Hao
Allergens, a common trigger of asthma, can lead to increased levels of reactive oxygen species (ROS) and subsequent DNA damage. However, the repair mechanism of DNA damage caused by oxidative stress in allergen-induced asthma is less known. We explored the mechanism by which topoisomerase 1 binding arginine/serine rich protein (TOPORS) regulates small ubiquitin-related modifier 1 (SUMO1) modification of TOP1 to repair DNA damage induced by ovalbumin (OVA). We tested the expression level of TOP1 in asthmatic and healthy children. OVA-induced mouse asthma model was used for further validation. The level of SUMO1-TOP1 in macrophages was studied by immunoprecipitation. The expression of TOP1 was increased in asthmatic children. The expression of TOP1 and γ Histone 2AX (γH2AX) were increased in the lung tissue of asthmatic mice. In OVA-induced macrophages, the levels of TOP1 and γH2AX were increased, while knockdown expression of TOP1 could reduce the level of γH2AX. The level of SUMO1-TOP1 in OVA-induced macrophages was increased. Interestingly, knockdown expression of TOPORS could reduce the levels of SUMO1-TOP1 in OVA-induced macrophages, while the levels of TOP1 and γH2AX were increased. Our results indicate that TOPORS regulates SUMO1 modification of TOP1 and plays an important role in the repair of DNA damage induced by OVA. DNA repair in asthma exacerbation could be a therapeutic target.
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CANCER LETTERS
·
2025
·
IF 10.1
Hongchengcheng Chen,Guihui Yu,Haodong Lin,Xiao Albert Zhou,Jiansong Liu,Haoyun Liu,Yefei Luo,Kaiqi Cheng,Zuchao Mao,Yujie Ma,Jun Wang,Kezhong Chen,Jiadong Wang,Yun Li
R-loop accumulation has emerged as a critical factor that induces DNA damage and compromises genomic integrity. However, the regulatory mechanisms governing the R-loop-induced DNA damage remain unclear. Here, FTSJ3 was determined to be a pivotal regulator of R-loop homeostasis and genomic stability. We demonstrated that FTSJ3 was specifically recruited to R-loop structures, where it prevented DNA damage by suppressing excessive R-loop formation. FTSJ3 expression was significantly upregulated in multiple cancer types, and its elevated expression levels correlated with unfavorable survival in patients with lung adenocarcinoma (LUAD). FTSJ3 depletion increased R-loop-dependent DNA damage. Inhibiting FTSJ3 expression sensitized lung cancer cells to cisplatin both in vitro and in vivo . FTSJ3 could be a genome guardian that limits R-loop-associated damage, suggesting its potential role as a cancer intervention therapeutic target and a predictive biomarker for chemotherapy responsiveness.
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ACS Sensors
·
2026
·
IF 10.9
Runcheng Liu,Jie Yan,Shujun Zhang,Wen Yang,Juan Li,Xiaoyan Sun,Lutao Du,Mingshun Jiang
DNA methylation has emerged as a pivotal molecular biomarker for early cancer diagnosis. Nevertheless, existing detection strategies remain limited by complex workflows, poor efficiency in trace DNA capture, and the inability to resolve both absolute concentration and methylation ratio simultaneously. Herein, we engineer a tilted fiber Bragg grating (TFBG) biosensor functionalized with Au@zeolitic imidazolate framework-8 (Au@ZIF-8) core-shell nanoparticle arrays. This architecture overcomes the diffusion-limited capture of conventional biosensors through a powerful hydrodynamic−plasmonic synergy. First, hydrodynamic stagnation flow efficiently preconcentrates trace DNA molecules onto the sensing interface. Subsequently, plasmon-enhanced dielectrophoresis provides an active trapping force, precisely localizing these molecules onto sensing hotspots. To enable multiparametric methylation profiling, a dual-recognition strategy was developed by integrating sequence-specific DNA hybridization with 5-methylcytosine (5mC) antibody binding. This approach allows for rapid (<15 min), amplification-free quantification of both methylated DNA concentration and methylation ratio in complex biological samples, with an ultralow detection limit of 6.9 × 102 copies/μL. Clinical validation using patient-derived samples demonstrates excellent diagnostic accuracy, achieving a receiver operating characteristic (ROC) area under the curve (AUC) of 0.941 through multilocus methylation analysis. This study establishes a robust, amplification- and label-free biosensing platform that integrates microfluidic manipulation with plasmonic nanoengineering, offering a powerful strategy for high-throughput, clinically translatable DNA methylation analysis in early cancer detection.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Manqing Zhang,Yufei Lan,Qu Yue,Jinjun He,Lei Li,Huan Zhang,Yaoyuan Dong,Yuankai Wang,Jiankun Lu,Zhijie Lu,Feiyunduo Hao,Sui Chen,Yixiao Jiang,Chao Zhang,Yan Zhao,Hongbo Guo
Alzheimer's disease (AD) pathological progression is intimately linked to microglial inflammatory activation mediated by the cGAS-STING pathway. Small interfering RNA targeting STING (siSTING) is a precise therapeutic to silence STING and interfere with this pathway, but its clinical translation is severely limited by serum nuclease degradation, inadequate blood-brain barrier (BBB) penetration, and suboptimal targeting. We constructed a lock-equipped six-helix DNA bundle for siSTING delivery. Prior to reaching AD lesions, siSTING was efficiently sequestered within the DNA bundle, ensuring its structural integrity; upon arrival at the lesion site, the carrier undergoes a conformational change in response to the high expression of CD64, thereby triggering the controlled release of encapsulated siSTING. Functional assessments showed this system significantly suppressed cGAS-STING activation, reduced cerebral Aβ plaque deposition, and promoted microglial polarization from M1 (proinflammatory) to M2 (anti-inflammatory). These effects ameliorated memory and learning deficits in AD model mice via enhanced neuroprotection, offering a novel platform for precise targeted therapy of AD.
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