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  • 1
    Online Resource
    Online Resource
    Unraveling the Plasma Protein Corona by Ultrasonic Cavitation Augments Active‐Transporting of Liposome in Solid Tumor
    Wiley ; 2023
    In:  Advanced Materials Vol. 35, No. 9 ( 2023-03)
    Details
    In: Advanced Materials, Wiley, Vol. 35, No. 9 ( 2023-03)
    Abstract: Ligand/receptor‐mediated targeted drug delivery has been widely recognized as a promising strategy for improving the clinical efficacy of nanomedicines but is attenuated by the binding of plasma protein on the surface of nanoparticles to form a protein corona. Here, it is shown that ultrasonic cavitation can be used to unravel surface plasma coronas on liposomal nanoparticles through ultrasound (US)‐induced liposomal reassembly. To demonstrate the feasibility and effectiveness of the method, transcytosis‐targeting‐peptide‐decorated reconfigurable liposomes (LPGLs) loaded with gemcitabine (GEM) and perfluoropentane (PFP) are developed for cancer‐targeted therapy. In the blood circulation, the targeting peptides are deactivated by the plasma corona and lose their targeting capability. Once they reach tumor blood vessels, US irradiation induces transformation of the LPGLs from nanodrops into microbubbles via liquid–gas phase transition and decorticate the surface corona by reassembly of the lipid membrane. The activated liposomes regain the capability to recognize the receptors on tumor neovascularization, initiate ligand/receptor‐mediated transcytosis, achieve efficient tumor accumulation and penetration, and lead to potent antitumor activity in multiple tumor models of patient‐derived tumor xenografts. This study presents an effective strategy to tackle the fluid biological barriers of the protein corona and develop transcytosis‐targeting liposomes for active tumor transport and efficient cancer therapy.
    Type of Medium: Online Resource
    ISSN: 0935-9648 , 1521-4095
    URL: Issue
    URL: Article
    DOI: 10.1002/adma.v35.9
    DOI: 10.1002/adma.202207271
    RVK:
    UA 1538
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1474949-X
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  • 2
    Online Resource
    Online Resource
    Lime and ammonium carbonate fumigation coupled with bio‐organic fertilizer application steered banana rhizosphere to assemble a unique microbiome against Panama disease
    Wiley ; 2019
    In:  Microbial Biotechnology Vol. 12, No. 3 ( 2019-05), p. 515-527
    Details
    In: Microbial Biotechnology, Wiley, Vol. 12, No. 3 ( 2019-05), p. 515-527
    Abstract: Microbiome plays a key role in determining soil suppressiveness against invading pathogens. Our previous study revealed that microbial community of bulk soil could be manipulated by lime and ammonium bicarbonate fumigation followed by biofertilizer application. However, the assembly of microbial community suppressive to banana Panama disease in the rhizosphere is still unclear. In this study, we used high‐throughput sequencing and quantitative PCR to explore the assembly of rhizosphere microbiome associated with banana Panama disease suppression in a two‐seasonal pot experiment. We found biofertilizer applied to lime and ammonium bicarbonate fumigated soil significantly ( P  〈  0.05) reduced the abundance of rhizosphere Fusarium oxysporum compared to biofertilizer applied to non‐fumigated soil. Principal coordinate analysis revealed that biofertilizer applied to lime and ammonium bicarbonate fumigated soil re‐shaped the rhizosphere bacterial community composition by increasing the phylogenetic relatedness, and stimulating indigenous microbes, for example , Gemmatimonas , Sphingomonas , Pseudomonas , Lysobacter and Bacillus . Co‐occurrence analysis revealed that potential species involved in disease suppression were more interrelated in disease‐suppressive soils. Taken together, lime and ammonium bicarbonate fumigation followed by biofertilizer application could induce banana rhizosphere to assemble beneficial microbes dominated consortia to suppress banana Panama disease.
    Type of Medium: Online Resource
    ISSN: 1751-7915 , 1751-7915
    URL: Issue
    URL: Article
    DOI: 10.1111/mbt2.2019.12.issue-3
    DOI: 10.1111/1751-7915.13391
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2406063-X
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  • 3
    Online Resource
    Online Resource
    Oxidized sodium alginate crosslinked silk fibroin composite scaffold for skin tissue engineering
    Wiley ; 2022
    In:  Journal of Biomedical Materials Research Part B: Applied Biomaterials Vol. 110, No. 12 ( 2022-12), p. 2667-2675
    Details
    In: Journal of Biomedical Materials Research Part B: Applied Biomaterials, Wiley, Vol. 110, No. 12 ( 2022-12), p. 2667-2675
    Abstract: Engineering skin substitutes represent a prospective source of advanced therapy in repairing severe traumatic wounds. Sodium alginate (SA) and silk fibroin (SF) are natural biomaterials, which are widely used in tissue engineering and other fields because of their low price, high safety, and good biocompatibility. However, SA itself degrades slowly, its degradation mode is difficult to control, and the degradation products are difficult to remove from the body because of its high molecular weight. Therefore, the composite scaffolds were prepared by freeze‐drying composite technology by using the Schiff base reaction between biocompatible SF and permeable oxidized sodium alginate (OSA). Sodium periodate was used as oxidant to modify SA. The results showed that higher oxidation degree of OSA could be obtained by increasing the proportion of oxidant, and the relative molecular weight of the oxidized products could also be reduced. The composite scaffolds were prepared by using sodium tetraborate as a crosslinking accelerator of the Schiff base reaction between OSA and SF. FT‐IR confirmed that the Schiff base group appeared in the material. In vitro biodegradation experiments showed that the biodegradation of the composite scaffolds was controllable, and the cytocompatibility experiment showed that the composite scaffolds had good biocompatibility.
    Type of Medium: Online Resource
    ISSN: 1552-4973 , 1552-4981
    URL: Issue
    URL: Article
    DOI: 10.1002/jbm.b.v110.12
    DOI: 10.1002/jbm.b.35119
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2130917-6
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    SETD8 C302R Mutation Revealed from Myofibroblastoma‐Discordant Monozygotic Twins Leads to p53/p21 Deficit and WEE1 Inhibitor Sensitivity
    Wiley ; 2020
    In:  Advanced Science Vol. 7, No. 19 ( 2020-10)
    Details
    In: Advanced Science, Wiley, Vol. 7, No. 19 ( 2020-10)
    Abstract: High‐throughput gene sequencing has identified various genetic variants as the culprits for some common hereditary cancers. However, the heritability of a substantial proportion of cancers remains unexplained, which may result from rare deleterious mutations hidden in a myriad of nonsense genetic variations. This poses a great challenge to the understanding of the pathology and thus the rational design of effective treatments for affected patients. Here, whole genome sequencing is employed in a representative case in which one monozygotic twin is discordant for lung inflammatory myofibroblastoma to disclose rare tumor‐related mutations. A missense single nucleotide variation rs61955126 T 〉 C in the lysine methyltransferase SETD8 (accession: NM_020382, SETD8 C302R ) is exposed. It is shown that SETD8 is vital for genomic integrity by promoting faithful DNA replication, and its C302R mutation downregulates the p53/p21 pathway. Importantly, the SETD8 C302R mutation significantly increases the sensitivity of cancer cells to WEE1 inhibition. Given that WEE1 inhibitors have shown great promise for clinical approval, these results impart a potential therapeutic approach using WEE1 inhibitor for cancer patients carrying the same mutation, and indicate that genome sequencing and genetic functional studies can be integrated into individualized therapies.
    Type of Medium: Online Resource
    ISSN: 2198-3844 , 2198-3844
    URL: Issue
    URL: Article
    DOI: 10.1002/advs.v7.19
    DOI: 10.1002/advs.202001041
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2808093-2
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  • 5
    Online Resource
    Online Resource
    Integrated transcriptomics, proteomics, and functional analysis to characterize the tissue‐specific small extracellular vesicle network of breast cancer
    Wiley ; 2023
    In:  MedComm Vol. 4, No. 6 ( 2023-12)
    Details
    In: MedComm, Wiley, Vol. 4, No. 6 ( 2023-12)
    Abstract: Small extracellular vesicles (sEVs) are essential mediators of intercellular communication within the tumor microenvironment (TME). Although the biological features of sEVs have been characterized based on in vitro culture models, recent evidence indicates significant differences between sEVs derived from tissue and those derived from in vitro models in terms of both content and biological function. However, comprehensive comparisons and functional analyses are still limited. Here, we collected sEVs from breast cancer tissues (T‐sEVs), paired normal tissues (N‐sEVs), corresponding plasma (B‐sEVs), and tumor organoids (O‐sEVs) to characterize their transcriptomic and proteomic profiles. We identified the actual cancer‐specific sEV signatures characterized by enriched cell adhesion and immunomodulatory molecules. Furthermore, we revealed the significant contribution of cancer‐associated fibroblasts in the sEV network within the TME. In vitro model‐derived sEVs did not entirely inherit the extracellular matrix‐ and immunity regulation‐related features of T‐sEVs. Also, we demonstrated the greater immunostimulatory ability of T‐sEVs on macrophages and CD8+ T cells compared to O‐sEVs. Moreover, certain sEV biomarkers derived from noncancer cells in the circulation exhibited promising diagnostic potential. This study provides valuable insights into the functional characteristics of tumor tissue‐derived sEVs, highlighting their potential as diagnostic markers and therapeutic agents for breast cancer.
    Type of Medium: Online Resource
    ISSN: 2688-2663 , 2688-2663
    URL: Issue
    URL: Article
    DOI: 10.1002/mco2.v4.6
    DOI: 10.1002/mco2.433
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 3021470-1
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  • 6
    Online Resource
    Online Resource
    High co‐expression of SLC7A11 and GPX4 as a predictor of platinum resistance and poor prognosis in patients with epithelial ovarian cancer
    Wiley ; 2022
    In:  BJOG: An International Journal of Obstetrics & Gynaecology Vol. 129, No. S2 ( 2022-11), p. 40-49
    Details
    In: BJOG: An International Journal of Obstetrics & Gynaecology, Wiley, Vol. 129, No. S2 ( 2022-11), p. 40-49
    Abstract: The aim was to assess the expression levels of SLC7A11 and GPX4 in relation to platinum resistance and prognosis in patients with epithelial ovarian cancer (EOC). Design A retrospective cohort study. Setting Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China. Population or Sample We included 192 eligible patients from hospital between January 2002 and December 2018. Methods We retrospectively analysed the medical records of patients with EOC. Surgical specimens of EOC were stained for SLC7A11 and GPX4. Survival analysis was performed using the Kaplan–Meier and Cox regression methods. Main Outcome Measures Clinical end points include platinum‐free interval (PFI), progression‐free survival (PFS) and overall survival (OS). Results Patients with high co‐expression levels of SLC7A11 and GPX4 had a 60‐fold higher risk of platinum resistance compared with those with low co‐expression (risk ratio, 60.46; 95% confidence interval [CI] 22.76–160.58; p   〈  0.001). Moreover, high co‐expression level of SLC7A11 and GPX4 was an independent prognostic factor for poor OS ( p   〈  0.001, hazard ratio [HR] 4.44, 95% CI, 2.77–7.14) and poor PFS ( p   〈  0.001, HR = 5.73, 95% CI, 3.86–8.73). For in vitro experiments, SLC7A11 and GPX4 expression were both upregulated in platinum‐resistant cells compared with their parental ovarian cancer cells, and siRNA‐induced SLC7A11 and GPX4 inhibition decreased platinum resistance. Conclusions High expression levels of SLC7A11 and GPX4 are associated with platinum resistance in EOC patients. High co‐expression of SLC7A11 and GPX4 may be a significant independent prognostic factor and a potential therapeutic target for platinum resistance in EOC patients.
    Type of Medium: Online Resource
    ISSN: 1470-0328 , 1471-0528
    URL: Issue
    URL: Article
    DOI: 10.1111/bjo.v129.s2
    DOI: 10.1111/1471-0528.17327
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2036469-6
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  • 7
    Online Resource
    Online Resource
    Adropin regulates hepatic glucose production via PP2A/AMPK pathway in insulin‐resistant hepatocytes
    Wiley ; 2020
    In:  The FASEB Journal Vol. 34, No. 8 ( 2020-08), p. 10056-10072
    Details
    In: The FASEB Journal, Wiley, Vol. 34, No. 8 ( 2020-08), p. 10056-10072
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v34.8
    DOI: 10.1096/fj.202000115RR
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 8
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    Online Resource
    The putative protein kinase Stk36 is essential for ciliogenesis and CSF flow by associating with Ulk4
    Wiley ; 2023
    In:  The FASEB Journal Vol. 37, No. 9 ( 2023-09)
    Details
    In: The FASEB Journal, Wiley, Vol. 37, No. 9 ( 2023-09)
    Abstract: Motile cilia lining on the ependymal cells are crucial for cerebrospinal fluid (CSF) flow and its dysfunction is often associated with hydrocephalus. Unc51‐like‐kinase 4 (Ulk4) was previously linked to CSF flow and motile ciliogenesis in mice, as the hypomorph mutant of Ulk4 ( Ulk4 tm1a/tm1a ) developed hydrocephalic phenotype resulted from defective ciliogenesis and disturbed ciliary motility, while the underling mechanism is largely obscure. Here, we report that serine/threonine kinase 36 (STK36), a paralog of ULK4, directly interacts with ULK4 and this was demonstrated by yeast two‐hybrid (Y2H) in yeast and coimmunoprecipitation (co‐IP) assays in HEK293T cells, respectively. The interaction region was confined to their respective N‐terminal kinase domain. The hypomorph mutant of Stk36 ( Stk36 tmE4−/− ) also developed progressive hydrocephalus postnatally and dysfunctional CSF flow, with multiple defects of motile cilia, including reduced ciliary number, disorganized ciliary orientation, defected axonemal structure and inconsistent base body (BB) orientation. Stk36 tmE4−/− also disturbed the expression of Foxj1 transcription factor and a range of other ciliogenesis‐related genes. All these morphological changes, motile cilia defects and transcriptional dysregulation in the Stk36 tmE4−/− are practically copied from that in Ulk4 tm1a/tm1a mice. Taken together, we conclude that both Stk36 and Ulk4 are crucial for CSF flow, they cooperate by direct binding with their kinase domain to regulate the Foxj1 transcription factor pathways for ciliogenesis and cilia function, not limited to CSF flow. The underlying molecular mechanism probably conserved in evolution and could be extended to other metazoans.
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v37.9
    DOI: 10.1096/fj.202300481R
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Genetic and epigenetic heterogeneity of epithelial ovarian cancer and the clinical implications for molecular targeted therapy
    Wiley ; 2016
    In:  Journal of Cellular and Molecular Medicine Vol. 20, No. 4 ( 2016-04), p. 581-593
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 20, No. 4 ( 2016-04), p. 581-593
    Abstract: Epithelial ovarian cancer ( EOC ) is the most lethal gynaecological malignancy, and tumoural heterogeneity ( TH ) has been blamed for treatment failure. The genomic and epigenomic atlas of EOC varies significantly with tumour histotype, grade, stage, sensitivity to chemotherapy and prognosis. Rapidly accumulating knowledge about the genetic and epigenetic events that control TH in EOC has facilitated the development of molecular‐targeted therapy. Poly (ADP‐ribose) polymerase (PARP) inhibitors, designed to target homologous recombination, are poised to change how breast cancer susceptibility gene (BRCA)‐related ovarian cancer is treated. Epigenetic treatment regimens being tested in clinical or preclinical studies could provide promising novel treatment approaches and hope for improving patient survival.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2016.20.issue-4
    DOI: 10.1111/jcmm.12771
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2076114-4
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  • 10
    Online Resource
    Online Resource
    The CTCF/LncRNA‐PACERR complex recruits E1A binding protein p300 to induce pro‐tumour macrophages in pancreatic ductal adenocarcinoma via directly regulating PTGS2 expression
    Wiley ; 2022
    In:  Clinical and Translational Medicine Vol. 12, No. 2 ( 2022-02)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 12, No. 2 ( 2022-02)
    Abstract: Tumour‐associated macrophages (TAMs) play an important role in promoting the progression of pancreatic ductal adenocarcinoma (PDAC). Here, we aimed to study the epigenetic mechanisms in regulating pro‐tumour M2‐polarised TAMs in the PDAC tumour microenvironment. Methods This study was conducted based on ex vivo TAMs isolated from PDAC tissues and in vitro THP1‐derived TAM model. RNA‐sequencing (RNA‐seq), assay for transposase‐accessible chromatin with sequencing and chromatin immunoprecipitation sequencing were performed to investigate gene expression, chromatin accessibility, transcription factor binding sites and histone modifications. Gene knockdown in THP1‐derived TAMs was performed with lentivirus, and the impact of THP1‐derived TAMs on invasion and metastasis ability of PDAC cells were investigated with in vitro and in vivo functional assays. RNA‐chromatin interaction was analysed by chromatin isolation through RNA purification with sequencing. RNA‐protein interaction was studied by RNA immunoprecipitation and RNA pull‐down. Results Our data showed that the transcription factor CTCF (CCCTC‐binding factor) was highly expressed in TAMs and predicted to be significantly enriched in hyper‐accessible chromatin regions when compared to monocytes. High infiltration of CTCF + TAMs was significantly associated with poor prognosis in PDAC patients. Knockdown of CTCF in THP1‐derived TAMs led to the down‐regulation of specific markers for M2‐polarised TAMs, including CD206 and CD163. When THP1‐derived TAMs with CTCF knockdown, they showed a decreased ability of invasion and metastasis. Further integrative analysis of multi‐omics data revealed that prostaglandin‐endoperoxide synthase 2 (PTGS2) and PTGS2 antisense NF‐κB1 complex‐mediated expression regulator RNA (PACERR) were critical downstream targets of CTCF and positively correlated with each other, which are closely situated on a chromosome. Knockdown of PACERR exhibited a similar phenotype as observed in CTCF knockdown THP1‐derived TAMs. Moreover, PACERR could directly bind to CTCF and recruit histone acetyltransferase E1A binding protein p300 to the promoter regions of PACERR and PTGS2, thereby enhancing histone acetylation and gene transcription, promoting the M2 polarization of TAMs in PDAC. Conclusions Our study demonstrated a novel epigenetic regulation mechanism of promoting pro‐tumour M2‐polarised TAMs in the PDAC tumour microenvironment.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v12.2
    DOI: 10.1002/ctm2.654
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2697013-2
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