We are analyzing https://link.springer.com/article/10.1186/s13046-019-1120-4.

Title:
Co-administration of 20(S)-protopanaxatriol (g-PPT) and EGFR-TKI overcomes EGFR-TKI resistance by decreasing SCD1 induced lipid accumulation in non-small cell lung cancer | Journal of Experimental & Clinical Cancer Research
Description:
Background Non-small cell lung cancer (NSCLC) patients with sensitive epidermal growth factor receptor (EGFR) mutations are successfully treated with EGFR tyrosine kinase inhibitors (EGFR-TKIs); however, resistance to treatment inevitably occurs. Given lipid metabolic reprogramming is widely known as a hallmark of cancer and intimately linked with EGFR-stimulated cancer growth. Activation of EGFR signal pathway increased monounsaturated fatty acids (MUFA) and lipid metabolism key enzyme Stearoyl-CoA Desaturase 1 (SCD1) expression. However the correlation between EGFR-TKI resistance and lipid metabolism remains to be determined. Methods In this study the differences in lipid synthesis between paired TKI-sensitive and TKI-resistant patient tissues and NSCLC cell lines were explored. Oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) was used to simulate a high lipid metabolic environment and detected the affection on the cytotoxic effect of TKIs (Gefitinib and osimertinib) in cell lines with EGFR-activating mutations. (20S)-Protopanaxatriol (g-PPT), an aglycone of ginsenosides, has been reported to be an effective lipid metabolism inhibitor, was used to inhibit lipid metabolism. Additionally, synergism in cytotoxic effects and signal pathway activation were evaluated using CCK-8 assays, Western blotting, flow cytometry, Edu assays, plate clone formation assays and immunofluorescence. Furthermore, two xenograft mouse models were used to verify the in vitro results. Results Gefitinib-resistant cells have higher lipid droplet content and SCD1 expression than Gefitinib-sensitive cells in both NSCLC cell lines and patient tissues. Additionally oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) abrogates the cytotoxic effect of both Gefitinib and osimertinib in cell lines with EGFR-activating mutations. As a reported effective lipid metabolism inhibitor, g-PPT significantly inhibited the expression of SCD1 in lung adenocarcinoma cells, and then down-regulated the content of intracellular lipid droplets. Combined treatment with Gefitinib and g-PPT reverses the resistance to Gefitinib and inhibits the activation of p-EGFR and the downstream signaling pathways. Conclusions Our findings uncover a link between lipid metabolic reprogramming and EGFR-TKI resistance, confirmed that combination target both EGFR and abnormal lipid metabolism maybe a promising therapy for EGFR-TKI resistance and highlighting the possibility of monitoring lipid accumulation in tumors for predicting drug resistance.
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Keywords {🔍}

cell, gefitinib, treatment, cells, cancer, gppt, lipid, lines, expression, scd, resistance, article, nsclc, egfr, metabolism, staining, panel, fig, google, scholar, lung, vehicle, effect, red, data, cas, tumor, pegfr, patients, content, combination, accumulation, mutations, hccgr, group, egfrtki, proliferation, experiments, nile, assessed, tkis, results, shown, lds, determined, mgkgday, exposed, growth, combined, performed,

Topics {✒️}

p-egfr/p-akt/p-erk tki-resistant egfr-mutant nsclc egfr-tki-sensitive cell lines antiapoptosis index bcl-xl egfr-tki-resistant cell lines mutation-specific egfr inhibitors mapk/erk pathway inhibitors receptor alpha-mediated expression heat-induced epitope retrieval egfr-stimulated cancer growth article google scholar oleic acid-induced activation molecular-targeted cancer therapies disrupting scd1-mediated synthesis article download pdf hcc827-luc xenograft model higher p-egfr/ki67 expression h1975-luc xenograft model egfr-tki-sensitive mutations anti-p-egfr1086 antibody lung cancer-initiating cells tki-resistant cell lines downstaging post-tki treatment received egfr-tki treatment reducing gefitinib-induced apoptosis reduce gefitinib-induced apoptosis concentrated depend g-ppt post-tki treatment specimens pi3k-akt signaling pathway full size image tki-resistant patient tissues post-tki treatment tissues oleic acid decreases egfr-mutated lung adenocarcinoma post-treatment patient tissue monounsaturated fatty acids enhance gefitinib-induced apoptosis paraffin-embedded tissue apoptosis indexes c-parp stearoyl-coa desaturase 1 stearoyl-coa desaturase stearoyl-coa desaturase-1 apoptosis related protein experimental animal center competitive reversible inhibitors lipid metabolism inhibitors fatty acid metabolism treated tki-resistant cells egfr-tkis hcc827-gr g-ppt drastically reduced

Schema {🗺️}

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            Lipid metabolism
            Lipid droplet
            SCD1
            Oleic acid
            Cancer Research
            Immunology
            Apoptosis
            Oncology
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      description:Non-small cell lung cancer (NSCLC) patients with sensitive epidermal growth factor receptor (EGFR) mutations are successfully treated with EGFR tyrosine kinase inhibitors (EGFR-TKIs); however, resistance to treatment inevitably occurs. Given lipid metabolic reprogramming is widely known as a hallmark of cancer and intimately linked with EGFR-stimulated cancer growth. Activation of EGFR signal pathway increased monounsaturated fatty acids (MUFA) and lipid metabolism key enzyme Stearoyl-CoA Desaturase 1 (SCD1) expression. However the correlation between EGFR-TKI resistance and lipid metabolism remains to be determined. In this study the differences in lipid synthesis between paired TKI-sensitive and TKI-resistant patient tissues and NSCLC cell lines were explored. Oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) was used to simulate a high lipid metabolic environment and detected the affection on the cytotoxic effect of TKIs (Gefitinib and osimertinib) in cell lines with EGFR-activating mutations. (20S)-Protopanaxatriol (g-PPT), an aglycone of ginsenosides, has been reported to be an effective lipid metabolism inhibitor, was used to inhibit lipid metabolism. Additionally, synergism in cytotoxic effects and signal pathway activation were evaluated using CCK-8 assays, Western blotting, flow cytometry, Edu assays, plate clone formation assays and immunofluorescence. Furthermore, two xenograft mouse models were used to verify the in vitro results. Gefitinib-resistant cells have higher lipid droplet content and SCD1 expression than Gefitinib-sensitive cells in both NSCLC cell lines and patient tissues. Additionally oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) abrogates the cytotoxic effect of both Gefitinib and osimertinib in cell lines with EGFR-activating mutations. As a reported effective lipid metabolism inhibitor, g-PPT significantly inhibited the expression of SCD1 in lung adenocarcinoma cells, and then down-regulated the content of intracellular lipid droplets. Combined treatment with Gefitinib and g-PPT reverses the resistance to Gefitinib and inhibits the activation of p-EGFR and the downstream signaling pathways. Our findings uncover a link between lipid metabolic reprogramming and EGFR-TKI resistance, confirmed that combination target both EGFR and abnormal lipid metabolism maybe a promising therapy for EGFR-TKI resistance and highlighting the possibility of monitoring lipid accumulation in tumors for predicting drug resistance.
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      keywords:
         NSCLC
         EGFR-TKI resistance
         Lipid metabolism
         Lipid droplet
         SCD1
         Oleic acid
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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      name:Xiao Wei
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Cancer Biology Research Center (Key Laboratory of the Ministry of Education), Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Yijuan Jia
      affiliation:
            name:Wuhan NO.1 Hospital
            address:
               name:Department of Obstetrics and Gynecology, Wuhan NO.1 Hospital, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Zheng Zhang
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Affiliated Yantai Yuhuangding Hospital of Qingdao University
            address:
               name:Department of Thoracic Surgery, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Bo Ai
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Xiaonian Cao
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Tao Guo
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Huazhong University of Science and Technology
            address:
               name:Collaborative Innovation Center of Hematology, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yongde Liao
      affiliation:
            name:Huazhong University of Science and Technology
            address:
               name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Huazhong University of Science and Technology
            address:
               name:Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Collaborative Innovation Center of Hematology, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Cancer Biology Research Center (Key Laboratory of the Ministry of Education), Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Obstetrics and Gynecology, Wuhan NO.1 Hospital, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, People’s Republic of China
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Collaborative Innovation Center of Hematology, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
      name:Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China

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