FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2786818729> ?p ?o ?g. }

• W2786818729 endingPage "1036.e9" @default.
• W2786818729 startingPage "1024" @default.
• W2786818729 abstract "Background & AimsCeramide, a sphingolipid metabolite, affects T-cell signaling, induces apoptosis of cancer cells, and slows tumor growth in mice. However, it has not been used as a chemotherapeutic agent because of its cell impermeability and precipitation in aqueous solution. We developed a nanoliposome-loaded C6-ceremide (LipC6) to overcome this limitation and investigated its effects in mice with liver tumors.MethodsImmune competent C57BL/6 mice received intraperitoneal injections of carbon tetrachloride and intra-splenic injections of oncogenic hepatocytes. As a result, tumors resembling human hepatocellular carcinomas developed in a fibrotic liver setting. After tumors formed, mice were given an injection of LipC6 or vehicle via tail vein every other day for 2 weeks. This was followed by administration, also via tail vein, of tumor antigen-specific (TAS) CD8+ T cells isolated from the spleens of line 416 mice, and subsequent immunization by intraperitoneal injection of tumor antigen-expressing B6/WT-19 cells. Tumor growth was monitored with magnetic resonance imaging. Tumor apoptosis, proliferation, and AKT expression were analyzed using immunohistochemistry and immunoblots. Cytokine production, phenotype, and function of TAS CD8+ T cells and tumor-associated macrophages (TAMs) were studied with flow cytometry, real-time polymerase chain reaction (PCR), and ELISA. Reactive oxygen species (ROS) in TAMs and bone marrow-derived macrophages, induced by colony stimulating factor 2 (GMCSF or CSF2) or colony stimulating factor 1 (MCSF or CSF1), were detected using a luminescent assay.ResultsInjection of LipC6 slowed tumor growth by reducing tumor cell proliferation and phosphorylation of AKT, and increasing tumor cell apoptosis, compared with vehicle. Tumors grew more slowly in mice given the combination of LipC6 injection and TAS CD8+ T cells followed by immunization compared with mice given vehicle, LipC6, the T cells, or immunization alone. LipC6 injection also reduced numbers of TAMs and their production of ROS. LipC6 induced TAMs to differentiate into an M1 phenotype, which reduced immune suppression and increased activity of CD8+ T cells. These results were validated by experiments with bone marrow-derived macrophages induced by GMCSF or MCSF.ConclusionsIn mice with liver tumors, injection of LipC6 reduces the number of TAMs and the ability of TAMs to suppress the anti-tumor immune response. LipC6 also increases the anti-tumor effects of TAS CD8+ T cells. LipC6 might therefore increase the efficacy of immune therapy in patients with hepatocellular carcinoma. Ceramide, a sphingolipid metabolite, affects T-cell signaling, induces apoptosis of cancer cells, and slows tumor growth in mice. However, it has not been used as a chemotherapeutic agent because of its cell impermeability and precipitation in aqueous solution. We developed a nanoliposome-loaded C6-ceremide (LipC6) to overcome this limitation and investigated its effects in mice with liver tumors. Immune competent C57BL/6 mice received intraperitoneal injections of carbon tetrachloride and intra-splenic injections of oncogenic hepatocytes. As a result, tumors resembling human hepatocellular carcinomas developed in a fibrotic liver setting. After tumors formed, mice were given an injection of LipC6 or vehicle via tail vein every other day for 2 weeks. This was followed by administration, also via tail vein, of tumor antigen-specific (TAS) CD8+ T cells isolated from the spleens of line 416 mice, and subsequent immunization by intraperitoneal injection of tumor antigen-expressing B6/WT-19 cells. Tumor growth was monitored with magnetic resonance imaging. Tumor apoptosis, proliferation, and AKT expression were analyzed using immunohistochemistry and immunoblots. Cytokine production, phenotype, and function of TAS CD8+ T cells and tumor-associated macrophages (TAMs) were studied with flow cytometry, real-time polymerase chain reaction (PCR), and ELISA. Reactive oxygen species (ROS) in TAMs and bone marrow-derived macrophages, induced by colony stimulating factor 2 (GMCSF or CSF2) or colony stimulating factor 1 (MCSF or CSF1), were detected using a luminescent assay. Injection of LipC6 slowed tumor growth by reducing tumor cell proliferation and phosphorylation of AKT, and increasing tumor cell apoptosis, compared with vehicle. Tumors grew more slowly in mice given the combination of LipC6 injection and TAS CD8+ T cells followed by immunization compared with mice given vehicle, LipC6, the T cells, or immunization alone. LipC6 injection also reduced numbers of TAMs and their production of ROS. LipC6 induced TAMs to differentiate into an M1 phenotype, which reduced immune suppression and increased activity of CD8+ T cells. These results were validated by experiments with bone marrow-derived macrophages induced by GMCSF or MCSF. In mice with liver tumors, injection of LipC6 reduces the number of TAMs and the ability of TAMs to suppress the anti-tumor immune response. LipC6 also increases the anti-tumor effects of TAS CD8+ T cells. LipC6 might therefore increase the efficacy of immune therapy in patients with hepatocellular carcinoma." @default.
• W2786818729 created "2018-02-23" @default.
• W2786818729 creator A5000097979 @default.
• W2786818729 creator A5000341566 @default.
• W2786818729 creator A5019875833 @default.
• W2786818729 creator A5032107158 @default.
• W2786818729 creator A5036968990 @default.
• W2786818729 creator A5037959368 @default.
• W2786818729 creator A5040371543 @default.
• W2786818729 creator A5043752774 @default.
• W2786818729 creator A5048785737 @default.
• W2786818729 creator A5059706312 @default.
• W2786818729 creator A5065871160 @default.
• W2786818729 creator A5065897181 @default.
• W2786818729 creator A5070298378 @default.
• W2786818729 creator A5086997032 @default.
• W2786818729 date "2018-03-01" @default.
• W2786818729 modified "2023-10-18" @default.
• W2786818729 title "Nanoliposome C6-Ceramide Increases the Anti-tumor Immune Response and Slows Growth of Liver Tumors in Mice" @default.
• W2786818729 cites W1480318795 @default.
• W2786818729 cites W1493940088 @default.
• W2786818729 cites W1497410183 @default.
• W2786818729 cites W1517564812 @default.
• W2786818729 cites W1923917571 @default.
• W2786818729 cites W1984484036 @default.
• W2786818729 cites W1984502708 @default.
• W2786818729 cites W1985199927 @default.
• W2786818729 cites W2000973050 @default.
• W2786818729 cites W2002250199 @default.
• W2786818729 cites W2012416768 @default.
• W2786818729 cites W2017792524 @default.
• W2786818729 cites W2020770410 @default.
• W2786818729 cites W2039475508 @default.
• W2786818729 cites W2042699075 @default.
• W2786818729 cites W2047740187 @default.
• W2786818729 cites W2051196306 @default.
• W2786818729 cites W2069412624 @default.
• W2786818729 cites W2071076441 @default.
• W2786818729 cites W2075738006 @default.
• W2786818729 cites W2076738925 @default.
• W2786818729 cites W2081127603 @default.
• W2786818729 cites W2082046754 @default.
• W2786818729 cites W2102724983 @default.
• W2786818729 cites W2106160782 @default.
• W2786818729 cites W2119305519 @default.
• W2786818729 cites W2122522101 @default.
• W2786818729 cites W2123318646 @default.
• W2786818729 cites W2131774025 @default.
• W2786818729 cites W2134601695 @default.
• W2786818729 cites W2143766145 @default.
• W2786818729 cites W2165610535 @default.
• W2786818729 cites W2169549127 @default.
• W2786818729 cites W2284593700 @default.
• W2786818729 cites W2494328932 @default.
• W2786818729 cites W334309946 @default.
• W2786818729 cites W4211105405 @default.
• W2786818729 cites W4211221095 @default.
• W2786818729 cites W4231345949 @default.
• W2786818729 cites W4246793538 @default.
• W2786818729 doi "https://doi.org/10.1053/j.gastro.2017.10.050" @default.
• W2786818729 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5908238" @default.
• W2786818729 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29408569" @default.
• W2786818729 hasPublicationYear "2018" @default.
• W2786818729 type Work @default.
• W2786818729 sameAs 2786818729 @default.
• W2786818729 citedByCount "96" @default.
• W2786818729 countsByYear W27868187292018 @default.
• W2786818729 countsByYear W27868187292019 @default.
• W2786818729 countsByYear W27868187292020 @default.
• W2786818729 countsByYear W27868187292021 @default.
• W2786818729 countsByYear W27868187292022 @default.
• W2786818729 countsByYear W27868187292023 @default.
• W2786818729 crossrefType "journal-article" @default.
• W2786818729 hasAuthorship W2786818729A5000097979 @default.
• W2786818729 hasAuthorship W2786818729A5000341566 @default.
• W2786818729 hasAuthorship W2786818729A5019875833 @default.
• W2786818729 hasAuthorship W2786818729A5032107158 @default.
• W2786818729 hasAuthorship W2786818729A5036968990 @default.
• W2786818729 hasAuthorship W2786818729A5037959368 @default.
• W2786818729 hasAuthorship W2786818729A5040371543 @default.
• W2786818729 hasAuthorship W2786818729A5043752774 @default.
• W2786818729 hasAuthorship W2786818729A5048785737 @default.
• W2786818729 hasAuthorship W2786818729A5059706312 @default.
• W2786818729 hasAuthorship W2786818729A5065871160 @default.
• W2786818729 hasAuthorship W2786818729A5065897181 @default.
• W2786818729 hasAuthorship W2786818729A5070298378 @default.
• W2786818729 hasAuthorship W2786818729A5086997032 @default.
• W2786818729 hasBestOaLocation W27868187291 @default.
• W2786818729 hasConcept C142724271 @default.
• W2786818729 hasConcept C153911025 @default.
• W2786818729 hasConcept C167672396 @default.
• W2786818729 hasConcept C185592680 @default.
• W2786818729 hasConcept C190283241 @default.
• W2786818729 hasConcept C203014093 @default.
• W2786818729 hasConcept C2776964913 @default.
• W2786818729 hasConcept C2778019345 @default.
• W2786818729 hasConcept C2778690821 @default.
• W2786818729 hasConcept C502942594 @default.

• next