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Topics {✒️}

n-[3-chloro-4-fluorophenyl]-7-methoxy-6-[3-morpholinopropoxy]quinazolin-4- amine egfr-tki-resistant aldh1a1bright/cd44high csc gadd153-ccaat-enhancing binding protein-β net/cancer-types/lung-cancer ccaat/enhancer-binding protein beta jun n-terminal kinase csc-enriched gefitinib-resistant cells csc cell-mediated resistance gsc-enriched gefitinib-resistant cells egfr-mutant lung cancers ccaat-enhancing binding protein drug-resistant cancer cells article download pdf small-cell lung cancer reduce csc-mediated resistance aldh1a1bright/cd44high cell population egfr-tkis exposure influences tyrosine kinase inhibitors therapeutic anti-csc trans retinoic acid trans-retinoic acid receptor class-selective retinoids retinoic acid receptor potential therapeutic targets egfr-tkis maintenance therapy tris/acetate/edta pcr cell-mediated resistance aldh1a1-negative cell population cancer therapies egfr/wnt signaling pathways retinoic acid signaling lung cancer stem aldehyde dehydrogenase inhibitors cancer stem cell cancer stem cell full access high atra levels quantitative fluorescence pcr gata-binding factor 6 retinoic acid receptors cell death dis cancer drug resistance short-term gefitinib treatment promising therapeutic strategy aldh1a1bright/cd44high cscs linked tumor stem cell cancer stemness induced cancer stem cells aldh/nrf2 signaling privacy choices/manage cookies

Schema {🗺️}

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         headline:All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells
         description:The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). CSCs with ALDH1A1bright /CD44high expression contribute to the TKIs resistance in NSCLC/ADC cells. All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. We therefore investigated whether ATRA could circumvent the resistance to improve the response to gefitinib in NSCLC/ADC cells. Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry (FCM) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells.
         datePublished:2020-04-15T00:00:00Z
         dateModified:2020-04-15T00:00:00Z
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            ALDH1A1
            CD44
            EGFR tyrosine kinase inhibitors
            Non-small cell lung adenocarcinoma
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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      headline:All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells
      description:The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). CSCs with ALDH1A1bright /CD44high expression contribute to the TKIs resistance in NSCLC/ADC cells. All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. We therefore investigated whether ATRA could circumvent the resistance to improve the response to gefitinib in NSCLC/ADC cells. Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry (FCM) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells.
      datePublished:2020-04-15T00:00:00Z
      dateModified:2020-04-15T00:00:00Z
      pageStart:1
      pageEnd:9
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12885-020-06818-0
      keywords:
         All-trans retinoic acid
         ALDH1A1
         CD44
         EGFR tyrosine kinase inhibitors
         Non-small cell lung adenocarcinoma
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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            name:Liyang Wang
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            name:Huan Huang
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                     name:Department of Medical oncology, Wuming Hospital Affiliated to Guangxi Medical University, Nanning, China
                     type:PostalAddress
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      name:Liyang Wang
      affiliation:
            name:Medical School of University of Electronic Science and Technology of China
            address:
               name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
               type:PostalAddress
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      name:Huan Huang
      affiliation:
            name:Wuming Hospital Affiliated to Guangxi Medical University
            address:
               name:Department of Medical oncology, Wuming Hospital Affiliated to Guangxi Medical University, Nanning, China
               type:PostalAddress
            type:Organization
      name:Xin Li
      affiliation:
            name:Medical School of University of Electronic Science and Technology of China
            address:
               name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Pinjia Wang
      affiliation:
            name:Medical School of University of Electronic Science and Technology of China
            address:
               name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Kun Mi
      affiliation:
            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
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            type:Organization
      name:Jia Cheng
      affiliation:
            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
               type:PostalAddress
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      name:Huifen Liu
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            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Cuirong Gu
      affiliation:
            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Lingxiao Huang
      affiliation:
            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Jianming Huang
      affiliation:
            name:Sichuan Cancer Insititute
            address:
               name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
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      email:[email protected]
PostalAddress:
      name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
      name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
      name:Department of Medical oncology, Wuming Hospital Affiliated to Guangxi Medical University, Nanning, China
      name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
      name:Department of Medical oncology, Sichuan Cancer Hospital, Medical School of University of Electronic Science and Technology of China, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China
      name:Department of Biochemistry & Molecular Biology, Sichuan Cancer Insititute, Chengdu, People’s Republic of China

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