We are analyzing https://link.springer.com/article/10.1007/s10120-020-01096-y.

Title:
ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-κB pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer | Gastric Cancer
Description:
Background Long non-coding RNA (lncRNA) ASB16 antisense RNA 1 (ASB16-AS1) is recognized as an oncogene in several cancer types, but its relation to GC is unknown. Tripartite motif containing 37 (TRIM37) has been proven to accelerate the development of gastric cancer (GC), whereas the molecular mechanism assisted ASB16-AS1 and TRIM37 in regulating GC progression remains unclear. Methods Differentially expressed lncRNAs in GC samples were analyzed based on Gene Expression Omnibus (GEO) data. CCK-8 and colony formation assays were applied to determine the proliferative ability of GC cells. Stem cell-like phenotype of GC cells was assessed by sphere formation assay and flow cytometry analysis. Luciferase reporter assay, RNA immunoprecipitation (RIP), pulldown, and co-immunoprecipitation (Co-IP) were performed to verify the interplay of RNA molecules. Results ASB16-AS1 was upregulated in GC samples according to GEO data and qRT-PCR analysis. ASB16-AS1 strengthened the proliferative ability and stem cell-like characteristics in GC cells. More importantly, ASB16-AS1 encouraged GC cell growth in vivo. Mechanistically, ASB16-AS1 strengthened TRIM37 expression by sequestering miR-3918 and miR-4676-3p. ASB16-AS1 activated NF-kappa B (NF-κB) pathway by cooperating with ATM serine/threonine kinase (ATM) to induce TRIM37 phosphorylation. Conclusion In summary, ASB16-AS1 exerted oncogenic functions in GC through modulating TRIM37 expression at both mRNA and protein levels. Graphic abstract
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Keywords {🔍}

asbas, trim, cells, cancer, fig, cell, pubmed, mirp, article, google, scholar, atm, gastric, cas, proliferation, tumor, cisplatin, qrtpcr, data, pathway, expression, overexpression, analysis, nfκb, stemness, resistance, rna, detected, assay, zhang, study, western, treatment, tissues, blot, central, lncrna, mrna, knockdown, promotes, normal, lncrnas, ges, samples, cck, wang, progression, growth, metastasis, liu,

Topics {✒️}

activating c-myc/nampt/sirt1-dependent foxo1 tgf-β-induced epithelial-mesenchymal transition sdpr-modulated positive-feedback loop activating wnt/β-catenin pathway lncrna xist/mir-200c regulates cops7a-mediated nf-κb pathway large-scale clip-seq data asb16-as1 activated nf-kappa nf-κb pathway-related proteins oct1-induced transcriptional activation induce nf-kappab activation induces epithelial-mesenchymal transition inactivating nf-kappab signaling nf-kappab signaling pathway endogenously sponging mir-204-5p asb16-as1-silenced gc cells activate nf-κb pathway cytoplasmic nf-kappab signaling trim37-wt/mut luciferase reporters spf-grade animal lab qrt-pcr detected asb16-as1 pi3k/akt signaling pathway quantitative real-time pcr asb16-as1 synergistically worked asb16-as1 synergistically work biotin-labeled asb16-as1 nf-κb pathway activity regulate nf-κb pathway silencing asb16-as1 reduced trim37-mediated gc progression asb16-as1 reduced flag-atm asb16-as1 accelerated proliferation asb16-as1 hindered proliferation generate asb16-as1-mut atm serine/threonine kinase modulating mir-22/net1 axis lncrna hoxc-as3 asb16-as1-wt/mut asb16-as1 knockdown blocked epithelial-mesenchymal transition regulating mir-1827/fzd4 axis asb16-as1 biotin probe cancer cell int modulate mir-22/net1 axis mir-370-3p/mir-1296-5p asb16-as1 knockdown caused exogenous ha-tagged trim37 nf-kappab pathway asb16-as1/trim37 signaling asb16-as1 depletion reduced

Schema {🗺️}

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         description:Long non-coding RNA (lncRNA) ASB16 antisense RNA 1 (ASB16-AS1) is recognized as an oncogene in several cancer types, but its relation to GC is unknown. Tripartite motif containing 37 (TRIM37) has been proven to accelerate the development of gastric cancer (GC), whereas the molecular mechanism assisted ASB16-AS1 and TRIM37 in regulating GC progression remains unclear. Differentially expressed lncRNAs in GC samples were analyzed based on Gene Expression Omnibus (GEO) data. CCK-8 and colony formation assays were applied to determine the proliferative ability of GC cells. Stem cell-like phenotype of GC cells was assessed by sphere formation assay and flow cytometry analysis. Luciferase reporter assay, RNA immunoprecipitation (RIP), pulldown, and co-immunoprecipitation (Co-IP) were performed to verify the interplay of RNA molecules. ASB16-AS1 was upregulated in GC samples according to GEO data and qRT-PCR analysis. ASB16-AS1 strengthened the proliferative ability and stem cell-like characteristics in GC cells. More importantly, ASB16-AS1 encouraged GC cell growth in vivo. Mechanistically, ASB16-AS1 strengthened TRIM37 expression by sequestering miR-3918 and miR-4676-3p. ASB16-AS1 activated NF-kappa B (NF-κB) pathway by cooperating with ATM serine/threonine kinase (ATM) to induce TRIM37 phosphorylation. In summary, ASB16-AS1 exerted oncogenic functions in GC through modulating TRIM37 expression at both mRNA and protein levels.
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      description:Long non-coding RNA (lncRNA) ASB16 antisense RNA 1 (ASB16-AS1) is recognized as an oncogene in several cancer types, but its relation to GC is unknown. Tripartite motif containing 37 (TRIM37) has been proven to accelerate the development of gastric cancer (GC), whereas the molecular mechanism assisted ASB16-AS1 and TRIM37 in regulating GC progression remains unclear. Differentially expressed lncRNAs in GC samples were analyzed based on Gene Expression Omnibus (GEO) data. CCK-8 and colony formation assays were applied to determine the proliferative ability of GC cells. Stem cell-like phenotype of GC cells was assessed by sphere formation assay and flow cytometry analysis. Luciferase reporter assay, RNA immunoprecipitation (RIP), pulldown, and co-immunoprecipitation (Co-IP) were performed to verify the interplay of RNA molecules. ASB16-AS1 was upregulated in GC samples according to GEO data and qRT-PCR analysis. ASB16-AS1 strengthened the proliferative ability and stem cell-like characteristics in GC cells. More importantly, ASB16-AS1 encouraged GC cell growth in vivo. Mechanistically, ASB16-AS1 strengthened TRIM37 expression by sequestering miR-3918 and miR-4676-3p. ASB16-AS1 activated NF-kappa B (NF-κB) pathway by cooperating with ATM serine/threonine kinase (ATM) to induce TRIM37 phosphorylation. In summary, ASB16-AS1 exerted oncogenic functions in GC through modulating TRIM37 expression at both mRNA and protein levels.
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      name:Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China
      name:Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China
      name:Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China
      name:Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China
      name:Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China

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