We are analyzing https://link.springer.com/article/10.1186/s13046-018-0734-2.

Title:
BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141 | Journal of Experimental & Clinical Cancer Research
Description:
Background miR-141 is up-regulated and plays crucial roles in nasopharyngeal carcinoma (NPC). However, the molecular mechanism underlying the dysregulation of miR-141 is still obscure. Methods Thus, the ChIP-PCR was performed to identify the c-Myc-binding sites in miR-141 and BRD7. qRT-PCR, western blot and immunohistochemistry assays were used to detect the expression of miR-141 and its up/down stream molecules. The rescue experiments on the c-Myc/miR-141 axis were performed in vitro and in vivo. Results Our results showed that the levels of mature miR-141, pre-miR-141 and pri-miR-141 were downregulated in c-Myc knockdown NPC cells. Meanwhile, c-Myc transactivates the expression of miR-141 by binding its promoter region. Moreover, BRD7 was identified as a co-factor of c-Myc to negatively regulate the activation of c-Myc/miR-141 axis, as well as a direct target of c-Myc. Moreover, restoration of miR-141 in c-Myc knockdown NPC cells notably rescued the effect of c-Myc on cell proliferation and tumor growth, as well as the blocking of PTEN/AKT pathway. Additionally, the expression of c-Myc was positively correlated with that of miR-141 and the clinical stages of NPC patients and negatively associated with the expression of BRD7. Our findings demonstrated that BRD7 expression and c-Myc activation forms a negative feedback loop to control the cell proliferation and tumor growth by targeting miR-141. Conclusions These observations provide new mechanistic insights into the dysregulation of miR-141 expression and a promising therapeutic option for NPC.
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Keywords {🔍}

cmyc, brd, expression, cells, npc, pubmed, cell, article, knockdown, google, scholar, transcription, fig, cas, tumor, promoter, protein, central, zhou, cancer, growth, dilution, proliferation, assays, liu, control, china, pathway, significantly, activity, activation, feedback, nasopharyngeal, additional, data, loop, file, controls, usa, pten, analysis, qrtpcr, results, patients, level, hek, table, zhang, performed, western,

Topics {✒️}

pires2-egfp/2flag-c-myc plasmid pires2-egfp/2flag-c-myc helix-loop-helix zipper protein basic-helix–loop–helix chip 10-putative c-myc-binding sites 5-putative c-myc-binding sites c-myc knockdown stable 5-8f sequence-specific dna-binding complex primary antibody anti-c-myc c-myc-overexpressing hek293 cells basic-helix–loop–helix predicted c-myc-binding sites article download pdf g0/g1 population compared c-myc/mir-141 transcription axis dual-luciferase reporter kit myc-driven prostate cancer double-negative feedback loop mature hsa-mir-141-specific probe annexin v-pe c-myc nhe iii microrna-200c modulates epithelial c-myc/mir-141 axis nf-kb signaling pathway c-myc-binding sites c-myc observably enhanced c-myc-overexpressing 5-8f brd7-mediated cell proliferation c-myc knockdown 5-8f c-myc knockdown tumors c-myc knockdown cells monomeric c-myc protein cdk/rb/e2f pathway microrna/tp53 feedback circuitry c-myc knockdown controls c-myc interacting proteins c-myc bound directly pgl3-enhancer empty vector c-myc-driven malignancies genome-wide chromatin occupancy c-myc-binding profile c-myc significantly elevated 25 μg/ml propidium iodide bmc mol biol endogenous c-myc protein c-myc knockdown group c-myc knockdown decreased plate colony-forming efficiency regulates brca1-dependent transcription c-myc binds directly

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WebPage:
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         headline:BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141
         description:miR-141 is up-regulated and plays crucial roles in nasopharyngeal carcinoma (NPC). However, the molecular mechanism underlying the dysregulation of miR-141 is still obscure. Thus, the ChIP-PCR was performed to identify the c-Myc-binding sites in miR-141 and BRD7. qRT-PCR, western blot and immunohistochemistry assays were used to detect the expression of miR-141 and its up/down stream molecules. The rescue experiments on the c-Myc/miR-141 axis were performed in vitro and in vivo. Our results showed that the levels of mature miR-141, pre-miR-141 and pri-miR-141 were downregulated in c-Myc knockdown NPC cells. Meanwhile, c-Myc transactivates the expression of miR-141 by binding its promoter region. Moreover, BRD7 was identified as a co-factor of c-Myc to negatively regulate the activation of c-Myc/miR-141 axis, as well as a direct target of c-Myc. Moreover, restoration of miR-141 in c-Myc knockdown NPC cells notably rescued the effect of c-Myc on cell proliferation and tumor growth, as well as the blocking of PTEN/AKT pathway. Additionally, the expression of c-Myc was positively correlated with that of miR-141 and the clinical stages of NPC patients and negatively associated with the expression of BRD7. Our findings demonstrated that BRD7 expression and c-Myc activation forms a negative feedback loop to control the cell proliferation and tumor growth by targeting miR-141. These observations provide new mechanistic insights into the dysregulation of miR-141 expression and a promising therapeutic option for NPC.
         datePublished:2018-03-20T00:00:00Z
         dateModified:2018-03-20T00:00:00Z
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         keywords:
            Nasopharyngeal carcinoma
            BRD7
            C-Myc
            Feedback loop
            miR-141
            AKT pathway
            Cancer Research
            Immunology
            Apoptosis
            Oncology
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ScholarlyArticle:
      headline:BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141
      description:miR-141 is up-regulated and plays crucial roles in nasopharyngeal carcinoma (NPC). However, the molecular mechanism underlying the dysregulation of miR-141 is still obscure. Thus, the ChIP-PCR was performed to identify the c-Myc-binding sites in miR-141 and BRD7. qRT-PCR, western blot and immunohistochemistry assays were used to detect the expression of miR-141 and its up/down stream molecules. The rescue experiments on the c-Myc/miR-141 axis were performed in vitro and in vivo. Our results showed that the levels of mature miR-141, pre-miR-141 and pri-miR-141 were downregulated in c-Myc knockdown NPC cells. Meanwhile, c-Myc transactivates the expression of miR-141 by binding its promoter region. Moreover, BRD7 was identified as a co-factor of c-Myc to negatively regulate the activation of c-Myc/miR-141 axis, as well as a direct target of c-Myc. Moreover, restoration of miR-141 in c-Myc knockdown NPC cells notably rescued the effect of c-Myc on cell proliferation and tumor growth, as well as the blocking of PTEN/AKT pathway. Additionally, the expression of c-Myc was positively correlated with that of miR-141 and the clinical stages of NPC patients and negatively associated with the expression of BRD7. Our findings demonstrated that BRD7 expression and c-Myc activation forms a negative feedback loop to control the cell proliferation and tumor growth by targeting miR-141. These observations provide new mechanistic insights into the dysregulation of miR-141 expression and a promising therapeutic option for NPC.
      datePublished:2018-03-20T00:00:00Z
      dateModified:2018-03-20T00:00:00Z
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      pageEnd:14
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s13046-018-0734-2
      keywords:
         Nasopharyngeal carcinoma
         BRD7
         C-Myc
         Feedback loop
         miR-141
         AKT pathway
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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