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  • Oxford University Press (OUP)  (6)
  • 1
    Online Resource
    Online Resource
    Indolocarbazole alkaloid Loonamycin A inhibits triple-negative breast cancer cell stemness and Notch signalling
    Oxford University Press (OUP) ; 2023
    In:  Journal of Pharmacy and Pharmacology Vol. 75, No. 4 ( 2023-04-07), p. 523-532
    Details
    In: Journal of Pharmacy and Pharmacology, Oxford University Press (OUP), Vol. 75, No. 4 ( 2023-04-07), p. 523-532
    Abstract: Enrichment for therapy-resistant cancer stem cells hampers the treatment of triple-negative breast cancer. Targeting these cells via suppression of Notch signalling can be a potential therapeutic strategy. This study aimed to uncover the mode of action of a new indolocarbazole alkaloid loonamycin A against this incurable disease. Methods The anticancer effects were examined in triple-negative breast cancer cells using in vitro methods, including cell viability and proliferation assays, wound-healing assay, flow cytometry and mammosphere formation assay. RNA-seq technology was used to analyse the gene expression profiles in loonamycin A-treated cells. Real-time RT-PCR and western blot were to evaluate the inhibition of Notch signalling. Key findings Loonamycin A has stronger cytotoxicity than its structural analog rebeccamycin. Besides inhibiting cell proliferation and migration, loonamycin A reduced CD44high/CD24low/− sub-population, mammosphere formation, as well as the expression of stemness-associated genes. Co-administration of loonamycin A enhanced antitumour effects of paclitaxel by inducing apoptosis. RNA sequencing results showed that loonamycin A treatment caused the inhibition of Notch signalling, accompanied by the decreased expression of Notch1 and its targeted genes. Conclusions These results reveal a novel bioactivity of indolocarbazole-type alkaloids and provide a promising Notch-inhibiting small molecular candidate for triple-negative breast cancer therapy.
    Type of Medium: Online Resource
    ISSN: 0022-3573 , 2042-7158
    URL: Article
    DOI: 10.1093/jpp/rgad007
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2041988-0
    detail.hit.zdb_id: 2050532-2
    SSG: 15,3
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  • 2
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    Online Resource
    KLF2+ stemness maintains human mesenchymal stem cells in bone regeneration
    Oxford University Press (OUP) ; 2020
    In:  Stem Cells Vol. 38, No. 3 ( 2020-03-01), p. 395-409
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 38, No. 3 ( 2020-03-01), p. 395-409
    Abstract: Mesenchymal stem cells (MSCs), which are undifferentiated stem cells with the property of stemness and the potential to differentiate into multiple lineages, including osteoblasts, have attracted a great deal of attention in bone tissue engineering. Consistent with the heterogeneity of MSCs, various surface markers have been used. However, it is still unclear which markers of MSCs are best for cell amplification in vitro and later bone regeneration in vivo. Krüppel-like Factor 2 (KLF2) is an important indicator of the stemness of human MSCs (hMSCs) and as early vascularization is also critical for bone regeneration, we used KLF2 as a novel in vitro marker for MSCs and investigated the angiogenesis and osteogenesis between KLF2+ MSCs and endothelial cells (ECs). We found a synergistic interaction between hMSCs and human umbilical vein ECs (HUVECs) in that KLF2+ stemness-maintained hMSCs initially promoted the angiogenesis of HUVECs, which in turn more efficiently stimulated the osteogenesis of hMSCs. In fact, KLF2+ hMSCs secreted angiogenic factors initially, with some of the cells then differentiating into pericytes through the PDGF-BB/PDGFR-β signaling pathway, which improved blood vessel formation. The matured HUVECs in turn synergistically enhanced the osteogenesis of KLF2+ hMSCs through upregulated vascular endothelial growth factor. A three-dimensional coculture model using cell-laden gelatin methacrylate (GelMA) hydrogel further confirmed these results. This study provides insight into the stemness-directed synergistic interaction between hMSCs and HUVECs, and our results will have a profound impact on further strategies involving the application of KLF2+ hMSC/HUVEC-laden GelMA hydrogel in vascular network bioengineering and bone regeneration.
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1002/stem.3120
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2030643-X
    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
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  • 3
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    OCIAD2 suppressed tumor growth and invasion via AKT pathway in Hepatocelluar carcinoma
    Oxford University Press (OUP) ; 2017
    In:  Carcinogenesis Vol. 38, No. 9 ( 2017-09-01), p. 910-919
    Details
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 38, No. 9 ( 2017-09-01), p. 910-919
    Type of Medium: Online Resource
    ISSN: 0143-3334 , 1460-2180
    URL: Article
    DOI: 10.1093/carcin/bgx073
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 1474206-8
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  • 4
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    Characterization of p38 MAPK isoforms for drug resistance study using systems biology approach
    Oxford University Press (OUP) ; 2014
    In:  Bioinformatics Vol. 30, No. 13 ( 2014-07-01), p. 1899-1907
    Details
    In: Bioinformatics, Oxford University Press (OUP), Vol. 30, No. 13 ( 2014-07-01), p. 1899-1907
    Abstract: Motivation: p38 mitogen-activated protein kinase activation plays an important role in resistance to chemotherapeutic cytotoxic drugs in treating multiple myeloma (MM). However, how the p38 mitogen-activated protein kinase signaling pathway is involved in drug resistance, in particular the roles that the various p38 isoforms play, remains largely unknown. Method: To explore the underlying mechanisms, we developed a novel systems biology approach by integrating liquid chromatography–mass spectrometry and reverse phase protein array data from human MM cell lines with computational pathway models in which the unknown parameters were inferred using a proposed novel algorithm called modularized factor graph. Results: New mechanisms predicted by our models suggest that combined activation of various p38 isoforms may result in drug resistance in MM via regulating the related pathways including extracellular signal-regulated kinase (ERK) pathway and NFкB pathway. ERK pathway regulating cell growth is synergistically regulated by p38δ isoform, whereas nuclear factor kappa B (NFкB) pathway regulating cell apoptosis is synergistically regulated by p38α isoform. This finding that p38δ isoform promotes the phosphorylation of ERK1/2 in MM cells treated with bortezomib was validated by western blotting. Based on the predicted mechanisms, we further screened drug combinations in silico and found that a promising drug combination targeting ERK1/2 and NFκB might reduce the effects of drug resistance in MM cells. This study provides a framework of a systems biology approach to studying drug resistance and drug combination selection. Availability and implementation: RPPA experimental Data and Matlab source codes of modularized factor graph for parameter estimation are freely available online at http://ctsb.is.wfubmc.edu/publications/modularized-factor-graph.php Contact:  xizhou@wakehealth.edu or zhanglcq@swu.edu.cn Supplementary information:  Supplementary data are available at Bioinformatics online.
    Type of Medium: Online Resource
    ISSN: 1367-4811 , 1367-4803
    URL: Article
    DOI: 10.1093/bioinformatics/btu133
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 1468345-3
    SSG: 12
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  • 5
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    Decreased activity of RCAN1.4 is a potential risk factor for congenital heart disease in a Han Chinese population
    Oxford University Press (OUP) ; 2018
    In:  Protein & Cell Vol. 9, No. 12 ( 2018-12-01), p. 1039-1044
    Details
    In: Protein & Cell, Oxford University Press (OUP), Vol. 9, No. 12 ( 2018-12-01), p. 1039-1044
    Type of Medium: Online Resource
    ISSN: 1674-800X , 1674-8018
    URL: Article
    DOI: 10.1007/s13238-018-0525-8
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2543451-2
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  • 6
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    Functional linear regression for discretely observed data: from ideal to reality
    Oxford University Press (OUP) ; 2023
    In:  Biometrika Vol. 110, No. 2 ( 2023-05-15), p. 381-393
    Details
    In: Biometrika, Oxford University Press (OUP), Vol. 110, No. 2 ( 2023-05-15), p. 381-393
    Abstract: Despite extensive studies on functional linear regression, there exists a fundamental gap in theory between the ideal estimation from fully observed covariate functions and the reality that one can only observe functional covariates discretely with noise. The challenge arises when deriving a sharp perturbation bound for the estimated eigenfunctions in the latter case, which renders existing techniques for functional linear regression not applicable. We use a pooling method to attain the estimated eigenfunctions and propose a sample-splitting strategy to estimate the principal component scores, which facilitates the theoretical treatment for discretely observed data. The slope function is estimated by approximated least squares, and we show that the resulting estimator attains the optimal convergence rates for both estimation and prediction when the number of measurements per subject reaches a certain magnitude of the sample size. This phase transition phenomenon differs from the known results for the pooled mean and covariance estimation, and reveals the elevated difficulty in estimating the regression function. Numerical experiments, using simulated and real data examples, yield favourable results when compared with existing methods.
    Type of Medium: Online Resource
    ISSN: 0006-3444 , 1464-3510
    URL: Article
    DOI: 10.1093/biomet/asac053
    RVK:
    WA 15000
    RVK:
    QA 10000
    RVK:
    CL 1000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1119-8
    detail.hit.zdb_id: 1470319-1
    SSG: 12
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