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  • 1
    Online Resource
    Online Resource
    A novel LncRNA transcript, RBAT1, accelerates tumorigenesis through interacting with HNRNPL and cis-activating E2F3
    Springer Science and Business Media LLC ; 2020
    In:  Molecular Cancer Vol. 19, No. 1 ( 2020-12)
    Details
    In: Molecular Cancer, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2020-12)
    Abstract: Long non-coding RNAs (lncRNAs) have been identified as important epigenetic regulators that play critical roles in human cancers. However, the regulatory functions of lncRNAs in tumorigenesis remains to be elucidated. Here, we aimed to investigate the molecular mechanisms and potential clinical application of a novel lncRNA, retinoblastoma associated transcript-1 (RBAT1), in tumorigenesis. Methods RBAT1 expression was determined by real-time PCR in both retinoblastoma (Rb) and bladder cancer (BCa) cell lines and clinical tissues. Chromatin isolation using RNA purification (ChIRP) assays were performed to identify RBAT1-interacting proteins. Patient-derived xenograft (PDX) retinoblastoma models were established to test the therapeutic potential of RBAT1-targeting GapmeRs. Results Here, we found that RBAT1 expression was significantly higher in Rb and BCa tissues than that in adjacent tissues. Functional assays revealed that RBAT1 accelerated tumorigenesis both in vitro and in vivo . Mechanistically, RBAT1 recruited HNRNPL protein to E2F3 promoter, thereby activating E2F3 transcription. Therapeutically, GapmeR-mediated RBAT1 silencing significantly inhibited tumorigenesis in orthotopic xenograft retinoblastoma models derived from Rb cell lines and Rb primary cells. Conclusions RBAT1 overexpression upregulates a known oncogene, E2F3, via directly recruiting HNPNPL to its promoter and cis-activating its expression. Our finding provides a novel mechanism of lncRNA biology and provides potential targets for diagnosis and treatment of Rb and BCa.
    Type of Medium: Online Resource
    ISSN: 1476-4598
    URL: Article
    DOI: 10.1186/s12943-020-01232-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2091373-4
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  • 2
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    Online Resource
    Intraepithelial growth pattern for eyelid sebaceous carcinoma: a cohort of 214 patients from a single institution
    BMJ ; 2023
    In:  British Journal of Ophthalmology Vol. 107, No. 3 ( 2023-03), p. 324-330
    Details
    In: British Journal of Ophthalmology, BMJ, Vol. 107, No. 3 ( 2023-03), p. 324-330
    Abstract: To determine the distribution of three different intraepithelial growth patterns (pagetoid, bowenoid and papillary) in eyelid sebaceous carcinoma (SC) and correlate them with the clinical characteristics and prognosis. Methods A retrospective cohort study. The medical charts and pathological sections were retrospectively reviewed. All eligible patients were followed up for recurrence, metastasis and tumour-related mortality. The clinical significance of each intraepithelial growth pattern was determined by Cox regression. Results Of the 214 patients, 67 (31%) presented with intraepithelial invasion, among them, 34 (16%) were pagetoid, 27 (13%) were bowenoid and 6 (2.8%) were papillary. Patients of pagetoid intraepithelial spread showed significantly longer diagnostic delay (p=0.001) and more initial misdiagnoses of blepharitis (p=0.035). After a median follow-up period of 34.0 months, 67 (46%) patients in the non-intraepithelial group, 17 (50%) in the pagetoid group, 8 (30%) in the bowenoid group and 2 (33%) in the papillary group recurred. And 30 (20%) patients in the non-intraepithelial group, 9 (27%) in the pagetoid group and 4 (15%) in the bowenoid group developed metastasis. Moreover, 15 (10%) patients in the non-intraepithelial group, 6 (18%) in the pagetoid group and 1 (3.7%) in the bowenoid group died of SC. Cox regression indicated that pagetoid intraepithelial growth pattern was remarkably associated with increased chances of tumour-related mortality (HR=2.95, 95% CI 1.14 to 7.64, p=0.026). Conclusions Intraepithelial tumour invasion was presented in nearly one third of patients with eyelid SC. Pagetoid intraepithelial neoplasia, the predominant growth pattern, significantly increased the risk of tumour-related mortality. Meticulous histopathological intraepithelial examination is recommended for every patient of eyelid SC. Special attention should be paid to those with pagetoid invasion, who may require more intensive managements.
    Type of Medium: Online Resource
    ISSN: 0007-1161 , 1468-2079
    URL: Article
    DOI: 10.1136/bjophthalmol-2021-319789
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2023
    detail.hit.zdb_id: 1482974-5
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  • 3
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    Online Resource
    Novel insights into chromosomal conformations in cancer
    Springer Science and Business Media LLC ; 2017
    In:  Molecular Cancer Vol. 16, No. 1 ( 2017-12)
    Details
    In: Molecular Cancer, Springer Science and Business Media LLC, Vol. 16, No. 1 ( 2017-12)
    Type of Medium: Online Resource
    ISSN: 1476-4598
    URL: Article
    DOI: 10.1186/s12943-017-0741-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2091373-4
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  • 4
    Online Resource
    Online Resource
    〈p〉SKP2 targeted inhibition suppresses human uveal melanoma progression by blocking ubiquitylation of p27〈/p〉
    Informa UK Limited ; 2019
    In:  OncoTargets and Therapy Vol. Volume 12 ( 2019-05), p. 4297-4308
    Details
    In: OncoTargets and Therapy, Informa UK Limited, Vol. Volume 12 ( 2019-05), p. 4297-4308
    Type of Medium: Online Resource
    ISSN: 1178-6930
    URL: Journal
    URL: Article
    DOI: 10.2147/OTT
    DOI: 10.2147/OTT.S203888
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2495130-4
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  • 5
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    Online Resource
    Metformin promotes histone deacetylation of optineurin and suppresses tumour growth through autophagy inhibition in ocular melanoma
    Wiley ; 2022
    In:  Clinical and Translational Medicine Vol. 12, No. 1 ( 2022-01)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 12, No. 1 ( 2022-01)
    Abstract: To explore the therapeutic potential and the underlying mechanism of metformin, an adenosine monophosphate‐activated kinase (AMPK) activator, in ocular melanoma. Methods CCK8, transwell, and colony formation assays were performed to detect the proliferation and migration ability of ocular melanoma cells. A mouse orthotopic xenograft model was built to detect ocular tumor growth in vivo. Western blot, immunofluorescence, and electron microscopy were adopted to evaluate the autophagy levels of ocular melanoma cells, and high‐throughput proteomics and CUT & Tag assays were performed to analyze the candidate for autophagy alteration. Results Here, we revealed for the first time that a relatively low dose of metformin induced significant tumorspecific inhibition of the proliferation and migration of ocular melanoma cells both in vitro and in vivo. Intriguingly, we found that metformin significantly attenuated autophagic influx in ocular melanoma cells. Through high‐throughput proteomics analysis, we revealed that optineurin (OPTN), which is a key candidate for autophagosome formation and maturation, was significantly downregulated after metformin treatment. Moreover, excessive OPTN expression was associated with an unfavorable prognosis of patients. Most importantly, we found that a histone deacetylase, SIRT1, was significantly upregulated after AMPK activation, resulting in histone deacetylation in the OPTN promoter. Conclusions Overall, we revealed for the first time that metformin significantly inhibited the progression of ocular melanoma, and verified that metformin acted as an autophagy inhibitor through histone deacetylation of OPTN. This study provides novel insights into metformin ‐ guided suppression of ocular melanoma and the potential mechanism underlying the dual role of metformin in autophagy regulation.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v12.1
    DOI: 10.1002/ctm2.660
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2697013-2
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  • 6
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    Online Resource
    NSUN2‐mediated m 5 C RNA methylation dictates retinoblastoma progression through promoting PFAS mRNA stability and expression
    Wiley ; 2023
    In:  Clinical and Translational Medicine Vol. 13, No. 5 ( 2023-05)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 13, No. 5 ( 2023-05)
    Abstract: The precise temporal and spatial regulation of N 5 ‐methylcytosine (m 5 C) RNA modification plays essential roles in RNA metabolism, and is necessary for the maintenance of epigenome homeostasis. Howbeit, the mechanism underlying the m 5 C modification in carcinogenesis remains to be fully addressed. Methods Global and mRNA m 5 C levels were determined by mRNA isolation and anti‐m 5 C dot blot in both retinoblastoma (RB) cells and clinical samples. Orthotopic intraocular xenografts were established to examine the oncogenic behaviours of RB. Genome‐wide multiomics analyses were performed to identify the functional target of NSUN2, including proteomic analysis, transcriptome screening and m 5 C‐methylated RNA immunoprecipitation sequencing (m 5 C‐meRIP‐seq). Organoid‐based single‐cell analysis and gene‐correlation analysis were performed to verify the NSUN2/ALYREF/m 5 C‐PFAS oncogenic cascade. Results Herein, we report that NSUN2‐mediated m 5 C RNA methylation fuels purine biosynthesis during the oncogenic progression of RB. First, we discovered that global and mRNA m 5 C levels were significantly enriched in RBs compared to normal retinas. In addition, tumour‐specific NSUN2 expression was noted in RB samples and cell lines. Therapeutically, targeted correction of NSUN2 exhibited efficient therapeutic efficacy in RB both in vitro and in vivo. Through multiomics analyses, we subsequently identified phosphoribosylformylglycinamidine synthase (PFAS), a vital enzyme in purine biosynthesis, as a downstream candidate target of NSUN2. The reintroduction of PFAS largely reversed the inhibitory phenotypes in NSUN2‐deficient RB cells, indicating that PFAS was a functional downstream target of NSUN2. Mechanistically, we found that the m 5 C reader protein ALYREF was responsible for the recognition of the m 5 C modification of PFAS, increasing its expression by enhancing its RNA stability. Conclusions Conclusively, we initially demonstrated that NSUN2 is necessary for oncogenic gene activation in RB, expanding the current understanding of dynamic m 5 C function during tumour progression. As the NSUN2/ALYREF/m 5 C‐PFAS oncogenic cascade is an important RB trigger, our study suggests that a targeted m 5 C reprogramming therapeutic strategy may be a novel and efficient anti‐tumour therapy approach.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v13.5
    DOI: 10.1002/ctm2.1273
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2697013-2
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  • 7
    Online Resource
    Online Resource
    Spatiotemporal change of land use for deceased in Beijing since the mid-twentieth century
    Walter de Gruyter GmbH ; 2021
    In:  Open Geosciences Vol. 13, No. 1 ( 2021-01-13), p. 016-026
    Details
    In: Open Geosciences, Walter de Gruyter GmbH, Vol. 13, No. 1 ( 2021-01-13), p. 016-026
    Abstract: The land use for the deceased is not only for the dead but also for the living relatives. It competes with land use for living populations in urban areas through occupying a specific space of land. This article looks at this shared interest in humankind by mapping the land use for the deceased in the mid-twentieth century and modern Beijing and address the sustainability of future land use for dead in Beijing. Specifically, it clarifies the change of its area and location in the urban–regional structure and also considers the background factors. In the 1930s, the spatial distribution of cemeteries in the mid-twentieth century was mapped using the old topographic maps and also mainly using city government materials for modern times. A comparison of land use between the two periods shows that the spatial land use for the deceased continues to be the characteristics of traditional funeral values, Feng Shui philosophy, spatial separation of the dead, and the population, such as public cemeteries surrounding the built-up area. The city government reduced the pressure on land resources by encouraging land-saving burial such as undersea burial, which affects the value of funerals for citizens, resulting in an area of cemetery per urban population.
    Type of Medium: Online Resource
    ISSN: 2391-5447
    URL: Article
    DOI: 10.1515/geo-2020-0219
    Language: English
    Publisher: Walter de Gruyter GmbH
    Publication Date: 2021
    detail.hit.zdb_id: 2799881-2
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  • 8
    Online Resource
    Online Resource
    Generation of onco-enhancer enhances chromosomal remodeling and accelerates tumorigenesis
    Oxford University Press (OUP) ; 2020
    In:  Nucleic Acids Research Vol. 48, No. 21 ( 2020-12-02), p. 12135-12150
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 48, No. 21 ( 2020-12-02), p. 12135-12150
    Abstract: Chromatin remodeling impacts the structural neighborhoods and regulates gene expression. However, the role of enhancer-guided chromatin remodeling in the gene regulation remains unclear. Here, using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. Intriguingly, this novel CTCF-guided chromatin loop was ubiquitous in a cohort of tumor patients. In addition, a disruption in this chromosomal interaction prevented the histone acetyltransferase EP300 from embedding in the promoter of NTS and resulted in NTS silencing. Most importantly, in vitro and in vivo experiments showed that the ability of tumor formation was significantly suppressed via deletion of the enhancer by CRISPR-Cas9. These studies delineate a novel onco-enhancer guided epigenetic mechanism and provide a promising therapeutic concept for disease therapy.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkaa1051
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    A novel MYCN-YTHDF1 cascade contributes to retinoblastoma tumor growth by eliciting m6A -dependent activation of multiple oncogenes
    Springer Science and Business Media LLC ; 2023
    In:  Science China Life Sciences Vol. 66, No. 9 ( 2023-09), p. 2138-2151
    Details
    In: Science China Life Sciences, Springer Science and Business Media LLC, Vol. 66, No. 9 ( 2023-09), p. 2138-2151
    Type of Medium: Online Resource
    ISSN: 1674-7305 , 1869-1889
    URL: Article
    DOI: 10.1007/s11427-022-2288-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2546732-3
    detail.hit.zdb_id: 2133225-3
    SSG: 12
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  • 10
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    Online Resource
    Extrachromosomal circular DNA: biogenesis, structure, functions and diseases
    Springer Science and Business Media LLC ; 2022
    In:  Signal Transduction and Targeted Therapy Vol. 7, No. 1 ( 2022-10-02)
    Details
    In: Signal Transduction and Targeted Therapy, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2022-10-02)
    Abstract: Extrachromosomal circular DNA (eccDNA), ranging in size from tens to millions of base pairs, is independent of conventional chromosomes. Recently, eccDNAs have been considered an unanticipated major source of somatic rearrangements, contributing to genomic remodeling through chimeric circularization and reintegration of circular DNA into the linear genome. In addition, the origin of eccDNA is considered to be associated with essential chromatin-related events, including the formation of super-enhancers and DNA repair machineries. Moreover, our understanding of the properties and functions of eccDNA has continuously and greatly expanded. Emerging investigations demonstrate that eccDNAs serve as multifunctional molecules in various organisms during diversified biological processes, such as epigenetic remodeling, telomere trimming, and the regulation of canonical signaling pathways. Importantly, its special distribution potentiates eccDNA as a measurable biomarker in many diseases, especially cancers. The loss of eccDNA homeostasis facilitates tumor initiation, malignant progression, and heterogeneous evolution in many cancers. An in-depth understanding of eccDNA provides novel insights for precision cancer treatment. In this review, we summarized the discovery history of eccDNA, discussed the biogenesis, characteristics, and functions of eccDNA. Moreover, we emphasized the role of eccDNA during tumor pathogenesis and malignant evolution. Therapeutically, we summarized potential clinical applications that target aberrant eccDNA in multiple diseases.
    Type of Medium: Online Resource
    ISSN: 2059-3635
    URL: Article
    DOI: 10.1038/s41392-022-01176-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2886872-9
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