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  • Wiley  (4)
  • He, Yong  (4)
  • Lu, Conghua  (4)
  • Wang, Yubo  (4)
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  • Wiley  (4)
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  • 1
    Online Resource
    Online Resource
    Hexokinases II ‐mediated glycolysis governs susceptibility to crizotinib in ALK ‐positive non‐small cell lung cancer
    Wiley ; 2021
    In:  Thoracic Cancer Vol. 12, No. 23 ( 2021-12), p. 3184-3193
    Details
    In: Thoracic Cancer, Wiley, Vol. 12, No. 23 ( 2021-12), p. 3184-3193
    Abstract: Activation of ALK leads to a high level of aerobic glycolysis related to crizotinib insensitivity in anaplastic lymphoma kinase‐positive non‐small cell lung cancer (ALK + NSCLC). The strategy and mechanism of glycolysis inhibition in sensitizing ALK + NSCLC cells to crizotinib requires further investigation. Methods The levels of glycolysis in H3122 and H2228 cells were evaluated through detection of glucose consumption and lactate production. MTT assay was used to explore the effects of glycolytic inhibitors on crizotinib sensitivity, and the potential mechanism of action were detected by colony formation, Ki67 incorporation assay, transwell assay, small interfering RNA technology and western blot analysis. Results ALK + NSCLC cells exhibited significantly higher levels of glycolysis compared to ALK − NSCLC cells. Long‐term exposure to crizotinib could decrease the sensitivity of ALK + NSCLC cells to crizotinib via increasing the levels of glycolysis related to hexokinases II (HK2). Crizotinib in combination with glycolysis inhibitor 2‐deoxy‐D‐glucose (2DG) synergistically inhibited proliferation, glycolysis, colony formation and invasion ability of ALK + NSCLC cells. 2DG sensitization crizotinib might be associated with the inhibition of HK2‐mediated glycolysis and P‐ALK/AKT/mTOR signaling pathway in H3122 and H2228 cells. Conclusions These results indicate that HK2‐mediated glycolysis plays a crucial role in the increased tolerance of ALK + NSCLC cells to crizotinib. 2DG may sensitize ALK + NSCLC to crizotinib via suppression of HK2‐mediated glycolysis and the AKT/mTOR signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1759-7706 , 1759-7714
    URL: Issue
    URL: Article
    DOI: 10.1111/tca.v12.23
    DOI: 10.1111/1759-7714.14184
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2559245-2
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  • 2
    Online Resource
    Online Resource
    Aspirin sensitizes osimertinib‐resistant NSCLC cells in vitro and in vivo via Bim‐dependent apoptosis induction
    Wiley ; 2020
    In:  Molecular Oncology Vol. 14, No. 6 ( 2020-06), p. 1152-1169
    Details
    In: Molecular Oncology, Wiley, Vol. 14, No. 6 ( 2020-06), p. 1152-1169
    Abstract: Osimertinib, a third‐generation irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR‐TKI), provides marked clinical benefit for patients with EGFR‐activating mutations. Unfortunately, limited treatments exist for patients who acquire osimertinib resistance. We observed two ‘special’ patients who regained an antitumor response with osimertinib plus aspirin treatment. As previous data indicate that aspirin induces antiproliferative effects in tumor cells, we designed a preclinical study to explore whether aspirin combined with osimertinib could synergistically sensitize osimertinib‐resistant non‐small‐cell lung cancer (NSCLC) cells. The effects of combined treatment with osimertinib and aspirin on osimertinib‐resistant NSCLC cell lines were examined in vitro and in vivo . The combination of osimertinib and aspirin induced strong antiproliferative and proapoptotic effects in osimertinib‐resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression. Furthermore, Bim knockdown by siRNA significantly attenuated osimertinib resensitization by aspirin. In vivo , combination of aspirin and osimertinib significantly decreased tumor growth of PC‐9GROR cell xenografts. Data of patients with NSCLC who received osimertinib treatment at Daping Hospital between January 2015 and January 2019 were reviewed retrospectively. According to clinical data for 45 patients with NSCLC, retrospective analysis showed that the median progression‐free survival was significantly longer in the osimertinib plus aspirin group than in the osimertinib group. In summary, aspirin synergistically enhances the antitumor activity of osimertinib in osimertinib‐resistant lung cancer cells through promoting Bim‐dependent apoptosis. This combination therapy may be effective in overcoming acquired resistance to osimertinib and prolonging survival in patients with NSCLC.
    Type of Medium: Online Resource
    ISSN: 1574-7891 , 1878-0261
    URL: Issue
    URL: Article
    DOI: 10.1002/mol2.v14.6
    DOI: 10.1002/1878-0261.12682
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2322586-5
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  • 3
    Online Resource
    Online Resource
    Metformin‐sensitized NSCLC cells to osimertinib via AMPK‐dependent autophagy inhibition
    Wiley ; 2019
    In:  The Clinical Respiratory Journal Vol. 13, No. 12 ( 2019-12), p. 781-790
    Details
    In: The Clinical Respiratory Journal, Wiley, Vol. 13, No. 12 ( 2019-12), p. 781-790
    Abstract: The third‐generation epidermal growth factor receptor (EGFR) inhibitor osimertinib is a promising therapeutic option for patients with advanced non‐small‐cell lung cancer (NSCLC) in second‐line or first‐line treatment because of its applications in selectively inhibiting EGFR T790M and EGFR‐tyrosine kinase inhibitor sensitizing mutations. However, the activation of autophagy associated with osimertinib treatment may play a protective role in NSCLC cells injury induced by osimertinib. Objectives The aim of the present study was to study the effects of the osimertinib‐induced autophagy in NSCLC cells and whether metformin modulates the autophagy and enhances osimertinib sensitivity. Methods The effect of metformin on enhancing osimertinib sensitivity was examined in vitro and in vivo using MTT, BrdUrd incorporation assay, colony formation assay, invasion assay, flow cytometry analysis, western blot analysis and siRNA technique. Results In the present study, we confirmed that osimertinib induced pro‐survival autophagy in H1975 and PC‐9GR cells, and metformin further sensitized H1975 and PC‐9GR cells to osimertinib via inhibiting autophagy. The potential mechanism was that the continual activation of AMPK induced by metformin could inhibit autophagy in a time‐dependent manner. Conclusion Metformin inhibited autophagy and enhanced osimertinib sensitivity via inducing AMPK activation in a time‐dependent manner.
    Type of Medium: Online Resource
    ISSN: 1752-6981 , 1752-699X
    URL: Issue
    URL: Article
    DOI: 10.1111/crj.v13.12
    DOI: 10.1111/crj.13091
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2442214-9
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  • 4
    Online Resource
    Online Resource
    Predictive value of early kinetics of ctDNA combined with cfDNA and serum CEA for EGFR‐TKI treatment in advanced non‐small cell lung cancer
    Wiley ; 2022
    In:  Thoracic Cancer Vol. 13, No. 22 ( 2022-11), p. 3162-3173
    Details
    In: Thoracic Cancer, Wiley, Vol. 13, No. 22 ( 2022-11), p. 3162-3173
    Abstract: Circulating tumor DNA (ctDNA) has made a breakthrough as an early biomarker in operable early‐stage cancer patients. However, the function of ctDNA combined with cell‐free DNA (cfDNA) as a predictor in advanced non‐small cell lung cancer (NSCLC) remains unknown. Here, we explored its potential as a biomarker for predicting the efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR‐TKIs) in patients with advanced NSCLC. Methods A retrospective analysis was undertaken. Plasma collected from 51 patients with advanced NSCLC prior to and serially after starting treatment with EGFR‐TKIs was analyzed by next‐generation sequencing (NGS). The performance of ctDNA, cfDNA, and combining ctDNA with cfDNA were evaluated for their ability to predict survival outcomes. Results Patients with early undetectable ctDNA and increasing cfDNA had a markedly better progression‐free survival (PFS) ( p   〈  0.001) and overall survival (OS) ( p  = 0.001) than those with early detectable ctDNA and decreasing cfDNA. Patients with early ctDNA clearance were more likely to have the ctDNA persistent clearance ( p  = 0.006). The early clearance rate of ctDNA in the normal carcinoembryonic antigen (CEA) group was significantly higher than in the low and high groups ( p  = 0.028). Patients with greater CEA decline had a higher early clearance rate of ctDNA than those with minor CEA change ( p  = 0.016). Conclusions We based this study on ctDNA and cfDNA, explored its prognostic predictive ability, and combined CEA to monitor EGFR‐TKI efficacy. This study may provide new perspectives and insights into the precise treatment strategies for NSCLC patients.
    Type of Medium: Online Resource
    ISSN: 1759-7706 , 1759-7714
    URL: Issue
    URL: Article
    DOI: 10.1111/tca.v13.22
    DOI: 10.1111/1759-7714.14668
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2559245-2
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