ANALYTICAL CHEMISTRY
·
2026
·
IF 7.3
Li Xuegang,Zhao Xingyu,Zhang Jing,Zhou Xue,Zhang Yanan,Zhao Yong,Warren-Smith Stephen C.,Nguyen Linh Viet
Highly sensitive RNA detection at ultralow concentrations
remains
challenging for conventional surface plasmon resonance (SPR) biosensors
because low-molecularI biomolecules induce only weak effective refractive-index
perturbations within the limited evanescent-field penetration depth.
Here, we report a dual-scale gold nanoparticle (AuNP)–enhanced
fiber-optic SPR biosensor that overcomes this intrinsic limitation
through a mechanism-guided sandwich-type architecture. The sensor
employs a multimode fiber–single-mode fiber–multimode
fiber (MMF–SMF–MMF) configuration to enhance evanescent-field
excitation at the metal–dielectric interface. Plasmonic amplification
is achieved by decoupling probe immobilization and signal enhancement
into two AuNP populations with distinct roles: large AuNPs functionalized
with probe DNA form a stable, high-density recognition layer on the
gold-coated fiber surface, while small AuNPs conjugated with target
RNA act as mobile amplification units. Upon specific DNA–RNA
hybridization, a hierarchical plasmonic sandwich structure is formed
within the effective sensing volume, enabling synergistic enhancement
through near-field electromagnetic coupling and mass-loading effects.
Finite-element simulations and experiments consistently demonstrate
substantially stronger localized electromagnetic fields and higher
refractive-index sensitivity compared with bare gold films and monolayer
AuNP-modified SPR sensors. Importantly, the assay does not rely on
nucleic-acid amplification reactions or fluorescent labeling. The
sensor exhibits a linear response to RNA concentrations from 0 to
700 fM, achieving a sensitivity of 6.5 pm/fM and a detection limit
of 97 fM, corresponding to a 7.5-fold signal enhancement over conventional
single-layer AuNP-based SPR sensors. This work demonstrates that a
dual-scale AuNP-assisted sandwich architecture can effectively amplify
weak SPR responses from thiol-modified model RNA targets without requiring
nucleic-acid amplification reactions. Further optimization toward
direct detection of unmodified RNA in real biological samples will
be pursued in future work.
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Science China-Life Sciences
·
2026
·
IF 9.6
Cai Xia,Liu Yike,Li Jialuo,Zhao Zhuoran,Yao Xinyu,Zhai Zhihao,Liucong Mingmei,Liu Yujie,Wang Xue,Mochizuki Kazufumi,Tian Miao
Tetrahymena is a well-established ciliate model organism, known for its nuclear dualism and unique mechanism for transposon defense, wherein transposons are kept within the highly heterochromatinized micronucleus (MIC), which is transcriptionally inert except during meiosis. The discovery of preferential transcription in the meiotic MIC at regions enriched with transposons and the identification of MIC transcription regulatory proteins emphasize the necessity to elucidate the underlying mechanisms driving this process. In this study, we demonstrate that G/C-rich tracts are overrepresented in meiotic non-coding RNA (ncRNA) transcription regions and that RNA polymerase II (Pol II) is highly enriched at and around these tracts. Further analysis revealed that Pol II’s association with G/C-rich tracts is not abolished in cells lacking Rib1, a Mediator complex-associated protein essential for MIC ncRNA biogenesis. Nevertheless, in the absence of Rib1, Pol II showed abnormal association with the meiotic MIC chromatin, suggesting that Rib1 is critical for maintaining Pol II’s binding specificity. Through Rib1 truncation analysis, we found that the intrinsically disordered region, which contains putative phase-separating peptides, is crucial for its function. Disruption of phase-separation, either by deleting these peptides or by treating cells with a phase-separation disruption reagent, leads to aberrant localization of both Rib1 and Pol II on the MIC chromatin, implicating that Rib1 likely facilitates the MIC ncRNA transcription via phase-separation.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2025
·Vol. 23
·期 1
·1-23
·
IF 12.6
Xi Zhipeng,Xu Ning,Zhou Xiaobo,Chen Peng,He Yanwei,Wan Renwen,Zhang Longlong,Ding Zhipu,Cai Weiye,Chen Yisheng,Luo Zhiwen,Zhang Wei,Lin Chengshou,Chen Shuo,Zhao Zhijie,Liu Chao,Li Jingchi
Osteochondral defects pose significant challenges in joint health, leading to pain, decreased mobility, and substantial healthcare costs due to surgical interventions. This study aimed to develop and evaluate Si-A/PUE@HA composite hydrogels as scaffolding materials for cartilage tissue engineering, addressing the limitations of current treatment options. Utilizing a multi-step synthesis method that incorporates both chemical and physical crosslinking techniques, we assessed the hydrogels’ cytocompatibility, chondrogenic differentiation potential, immunomodulatory properties, and in vivo cartilage regeneration capabilities. In vitro results demonstrated high cell viability and proliferation rates of bone marrow mesenchymal stem cells (BMSCs) cultured in Si-A/PUE@HA hydrogels, with significant expression of chondrogenic markers such as Acan, Sox9, and Col2a1. Notably, the hydrogels exhibited a favorable immunomodulatory effect, promoting an anti-inflammatory M2 macrophage phenotype, which is crucial for tissue regeneration. In vivo studies confirmed substantial new tissue formation and integration with surrounding cartilage, as evidenced by micro-CT analysis, alongside excellent biocompatibility with no significant adverse effects observed in major organs over a 12-week period. Single-cell RNA sequencing analysis revealed a favorable immune microenvironment and enhanced chondrogenesis linked to hydrogel treatment. In conclusion, Si-A/PUE@HA hydrogels represent a promising biomaterial with potential applications in cartilage repair and regenerative medicine, warranting further investigation in larger clinical trials to validate their efficacy and safety for future therapeutic use. Graphical abstract
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Frontiers in Pharmacology
·
2025
·
IF 4.8
Miao Li,Na Gao,Lei Xu,Peng Ge,Nan Jiang,Yuhong Shang
Background: The natural compound paeonol exhibits therapeutic promise against cervical carcinoma, though its precise molecular mechanisms remain undefined.Methods: First, we treated human cervical cancer (HeLa) cells with different concentrations of paeonol. Cellular proliferation and apoptotic responses were evaluated via cell-counting kit 8 (CCK8) assays and flow cytometric analysis. Subsequent transcriptomic profiling employed RNA sequencing coupled with alternative splicing assessment to detect differentially expressed genes (DEGs). Protein interaction networks were established for pivotal DEGs, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment investigations. Clinical data pertinent to cervical cancer were retrieved from The Cancer Genome Atlas (TCGA). Prognostic model development incorporated Kaplan–Meier survival estimation, Least Absolute Shrinkage and Selection Operator (LASSO) regression, alongside univariate and multivariate COX proportional hazards analyses, with model accuracy subsequently assessed. Finally, Quantitative reverse transcription polymerase chain reaction (qRT-PCR) validated DEG expression.Results: Paeonol treatment suppressed proliferation while inducing apoptosis in HeLa cells. Transcriptomic and splicing analyses revealed 12 critical DEGs: NLRP1, FN1, NQO2, NREP, B4GALNT1, ANK3, FAM219A, ODF3B, MAPK15, EPGN, MUC1, and MEG3. Enrichment analyses indicated these DEGs principally associate with inflammatory processes and the biological regulation of cellular proliferation and apoptotic death. Analysis of clinical outcomes in 197 TCGA patients demonstrated significantly enhanced five-year survival probability within the low-risk cohort. FN1, NQO2, and ODF3B were incorporated into a prognostic signature following LASSO regression. Univariate and multivariate COX analyses identified T stage, tumor grade, and differential expression of these three genes as significant outcome predictors; the resultant prognostic model exhibited robust accuracy. qRT-PCR results corroborated the RNA sequencing data concerning DEG expression patterns.Conclusion: Paeonol modulates HeLa cell proliferation and apoptosis through regulation of 12 key genes, including FN1. This activity involves governing inflammatory responses alongside cellular proliferation, migration, and differentiation processes. These findings offer a theoretical foundation supporting paeonol’s potential clinical utility in cervical cancer management.
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YONSEI MEDICAL JOURNAL
·
2021
·
IF 2.759
Chunting Hu,Chen Li,Qiaoya Ma,Ruili Wang,Ya He,Hui Wang,Guogang Luo
Purpose Ischemic brain injury results in high mortality and serious neurologic morbidity. Here, we explored the role of SNHG15 in modulating neuronal damage and microglial inflammation after ischemia stroke. Materials and Methods The hypoxia/ischemia models were induced by middle cerebral artery occlusion in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Quantitative real-time PCR (qRT-PCR) and Western blot were conducted to determine the levels of SNHG15, miR-302a-3p, and STAT1/NF-κB. Moreover, gain- or loss-of functional assays of SNHG15 and miR-302a-3p were conducted. MTT assay was used to evaluate the viability of HT22 cells, and the apoptotic level was determined by flow cytometry. Furthermore, enzyme-linked immunosorbent assay was performed to detect oxidative stress and inflammatory mediators in the ischemia cortex and OGD/R-treated BV2 microglia. Results The SNHG15 and STAT1/NF-κB pathways were both distinctly up-regulated, while miR-302a-3p was notably down-regulated in the ischemia cortex. Additionally, overexpressing SNHG15 dramatically enhanced OGD/R-mediated neuronal apoptosis as well as the expression of oxidative stress and inflammation factors from microglia. In contrast, knocking down SNHG15 or overexpressing miR-302a-3p relieved OGD/R-mediated neuronal apoptosis and microglial activation. Moreover, the rescue experiment testified that overexpressing miR-302a-3p also attenuated SNHG15 up-regulation-induced effects. In terms of the mechanisms, SNHG15 sponged miR-302a-3p and activated STAT1/NF-κB as a competitive endogenous RNA, while miR-302a-3p targeted STAT1 and negatively regulated the STAT1/NF-κB pathway. Conclusion SNHG15 was up-regulated in the hypoxia/ischemia mouse or cell model. The inhibition of SNHG15 ameliorates ischemia/hypoxia-induced neuronal damage and microglial inflammation by regulating the miR-302a-3p/STAT1/NF-κB pathway.
研究领域:
神经科学
·
分子生物学
·
病理学
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Scientific Reports
·
2022
·Vol. 12
·期 1
·1-11
·
IF 4.996
Wan Yiting,Gu Cancan,Kong Jueying,Sui Jin,Zuo Ling,Song Yanhua,Chen Jing
Endometriosis (EMs) is one of the most frequent diseases of reproductive-age women and is characterized by the growth of endometrial tissues beyond the uterus. The enhanced proliferative and migratory potential of endometrial stromal cells (ESCs) plays an important role in the progression of EMs. Mounting studies have demonstrated that long noncoding RNAs (lncRNAs) exert an important role in regulating the development and progression of EMs. Given the aberrant expression of lncRNA ADAMTS9-AS1 in ectopic endometrium (ecEM), we investigated the biological effect of ADAMTS9-AS1 on ESC proliferation and migration and explored the underlying mechanism. The current data showed that ADAMTS9-AS1 expression was significantly upregulated in ecEM compared with eutopic endometrium (euEM) in patients with EMs and in a murine model of EMs. Functionally, ADAMTS9-AS1 knockdown in ectopic ESCs (EESCs) decreased cell viability and migration, whereas ADAMTS9-AS1 overexpression in normal ESCs (NESCs) enhanced cell viability and migration. More importantly, the effect of ADAMTS9-AS1 inhibition on decreasing ESC viability was significantly blocked by ferrostatin-1 (Fer-1, a ferroptosis inhibitor), and ADAMTS9-AS1 overexpression repressed erastin (a ferroptosis activator)-induced cell death. Furthermore, the regulatory role of ADAMTS9-AS1 in ferroptosis was defined and evidenced by increased reactive oxygen species (ROS) levels and malonyl dialdehyde (MDA) content and decreased expression of glutathione peroxidase 4 (GPX4) after ADAMTS9-AS1 inhibition. Mechanistically, ADAMTS9-AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-6516-5p to derepress the expression of GPX4, the critical repressor of ferroptosis. Taken together, these results demonstrate that upregulated ADAMTS9-AS1 accelerates ESC proliferation and migration by regulating miR-6516-5p/GPX4-dependent ferroptosis and may be a potential target for the treatment of EMs.
研究领域:
妇科学
·
分子生物学
·
细胞生物学
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BIOSENSORS & BIOELECTRONICS
·
2026
·
IF 11.8
Shuyun Weng,Hong Tao,Xu Luyun,Jianqing Ye,Wu Qiong,Min Fan,Xueliang Lin,Duo Lin,Ping Chen,Shangyuan Feng
Liver cancer (LC) is the third leading cause of cancer deaths worldwide, with the unsatisfactory clinical outcome due to high heterogeneity and metastasis. Unfortunately, it is still great challenging to achieve both effective screening and precise treatment of LC. Herein, a nanocomposite integrating dual-optical probes and gene regulation sequence was designed and prepared to simultaneously detect the novel gene biomarker and inhibit the metastasis-related gene function, achieving dual diagnostic and treatment functions for LC. Using the biosensing model based on surface-enhanced Raman spectroscopy (SERS) and fluorescence imaging, different expression of target circular RNA (cSMARCA5) in normal and LC cells can be characterized and quantified with an ultra-low limit of detection of 4.50 fM. Meanwhile, the specially-designed sequence loaded in the nanocomposite is capable of inhibiting the migration and invasion of LC cells in an in vitro model. Moreover, its ability of metastasis regulation for potential gene therapy can be further confirmed using optical imaging method via in vivo zebrafish transplantation tumor model. This work presents a dual-function nano-platform for simultaneous optical screening and gene treatment of LC, providing a unique strategy for precise medicine.
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GENOME BIOLOGY
·
2022
·Vol. 23
·期 1
·1-37
·
IF 17.906
Jiang Yongpeng,Huang Jie,Tian Kai,Yi Xiao,Zheng Haonan,Zhu Yi,Guo Tiannan,Ji Xiong
Background Mammalian cells have three types of RNA polymerases (Pols), Pol I, II, and III. However, the extent to which these polymerases are cross-regulated and the underlying mechanisms remain unclear.Results We employ genome-wide profiling after acute depletion of Pol I, Pol II, or Pol III to assess cross-regulatory effects between these Pols. We find that these enzymes mainly affect the transcription of their own target genes, while certain genes are transcribed by the other polymerases. Importantly, the most active type of crosstalk is exemplified by the fact that Pol III depletion affects Pol II transcription. Pol II genes with transcription changes upon Pol III depletion are enriched in diverse cellular functions, and Pol III binding sites are found near their promoters. However, these Pol III binding sites do not correspond to transfer RNAs. Moreover, we demonstrate that Pol III regulates Pol II transcription and chromatin binding of the facilitates chromatin transcription (FACT) complex to alter local chromatin structures, which in turn affects the Pol II transcription rate.Conclusion sOur results support a model suggesting that RNA polymerases show cross-regulatory effects: Pol III affects local chromatin structures and the FACT-Pol II axis to regulate the Pol II transcription rate at certain gene loci. This study provides a new perspective for understanding the dysregulation of Pol III in various tissues affected by developmental diseases.
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JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
·
2022
·Vol. 102
·期 10
·4054-4064
·
IF 4.125
Xianxian Dong,Yin Wan,Yanru Chen,Xiaojiang Wu,Yulong Zhang,Mengfei Deng,Wenqin Cai,Xiaodan Wu,Guiming Fu
BACKGROUND Tannase is an enzyme produced by microbial fermentation and is widely used in the food industry; however, the molecular mechanism of tannase production by Aspergillus has not yet been studied. This study was conducted to reveal the differences in Aspergillus carbonarius tannase enzymatic characterization, secondary structures and molecular mechanisms after treatment of the strain with atmospheric and room temperature plasma (ARTP). RESULTS The results showed that the specific activity of tannase was improved by ARTP treatment, and it showed higher thermostability and tolerance to metal ions and additives. The enzymatic characterization and molecular docking results indicated that tannase had a higher affinity and catalytic rate with tannic acid as a substrate after ARTP treatment. In addition, the docking results indicated that Aspergillus tannases may catalyze tannic acid by forming two hydrogen-bonding networks with neighboring residues. RNA-seq analysis indicated that changes in steroid biosynthesis, glutathione metabolism, glycerolipid metabolism, oxidative phosphorylation pathway and mitogen-activated protein kinase signaling pathways might be crucial reasons for the high production of tannase. CONCLUSION ARTP enhanced the yield and properties of A. carbonarius tannase by changing the enzyme structure and cell metabolism. This study provides a theoretical basis for elucidating the molecular mechanism underlying high production of Aspergillus tannases. © 2022 Society of Chemical Industry.
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Journal of Genetics and Genomics
·
2021
·
IF 4.275
Feifei Chen,Lei Guo,Jiehui Di,Man Li,Dong Dong,Dongsheng Pei
Numerous circular RNAs (circRNAs) have been identified as vital regulators in various cancers. The newly reported circular RNA ubiquitin-associated protein 2 (circUBAP2) is a critical player in cell growth and metastasis in various types of cancers, although its role in colorectal cancer (CRC) has yet to be fully elucidated. We find that circUBAP2 is upregulated in CRC tissues and cell lines to induce autophagy both in vitro and in vivo . The effects of circUBAP2 on migration, invasion, and proliferation may be partially related to autophagy. Mechanistically, we uncover that circUBAP2 can directly interact with miR-582-5p and subsequently act as a microRNA sponge to regulate the expression of the miR-582-5p target gene forkhead box protein O1 ( FOXO1 ) and downstream signaling molecules, which collectively advance the progression and metastasis of CRC. These results suggest that circUBAP2 acts as an oncogene via a novel circUBAP2/miR-582-5p/FOXO1 axis, providing a potential biomarker and therapeutic target for CRC management.
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MICROCHEMICAL JOURNAL
·
2021
·
IF 4.821
Yanhong Liu,Ping Chen,Kangkang Yu,Zhening Wu,Na Wang,Xiaoqi Yu
Heteroatoms doped carbon dots (CDs) have attracted extensive attention for their superior optical properties, facile preparation and multifunctional applications in environmental detection, cell imaging and gene delivery. Herein, Nitrogen and sulfur co-doped carbon dots (N,S-CDs) were synthesized directly from methyl cellulose (MC), l -cysteine ( l -cys) and ethylenediamine (EDA), showing excitation-dependent emission properties and relative high quantum yield (QY) of 12.3%. The obtained N,S-CDs are responsive to pH and temperature, suggesting pH- and temperature-dependent fluorescent features. Moreover, N,S-CDs are utilized to image and exhibit selective location inside the nucleus region both in living and fixed cells. Relative mechanisms have been explored by ribonuclease digestion testing and co-staining analysis with commercial nucleic acid dye. N,S-CDs show the specifical distribution in RNA-rich regions and positive response to RNA in cells. In brief, the developed N,S-CDs possess multi-faced application potency in pH sensing, temperature monitoring and RNA-selective imaging in cells.
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CANCER GENE THERAPY
·
2021
·Vol. 29
·期 1
·101-121
·
IF 5.987
Pan Jiongwei,Huang Gang,Yin Zhangyong,Cai Xiaoping,Gong Enhui,Li Yuling,Xu Cunlai,Ye Zaiting,Cao Zhuo,Cheng Wei
Significantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.
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