1,739,701 research outputs found

    Has_circ_0008583 modulates hepatocellular carcinoma progression through the miR-1301-3p/METTL3 pathway

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    Has_circ_0008583 is reported to be involved in the progression of hepatocellular carcinoma (HCC), while its biological role in HCC remains unclear. Here, the qRT-PCR was used to detect the expression of has_circ_0008583. The CCK-8 kit was performed to measure cell proliferation. The cell migration and invasion were evaluated by Transwell. A dual-luciferase reporter assay was performed to confirm the target combination between the genes in has_circ_0008583/miR-1301-3p/METTL3 axis. The in vivo role of has_circ_0008583 was verified by murine xenograft assay. Our data showed that hsa_circ_0008583 was upregulated in HCC tissues and cells. Hsa_circ_0008583 overexpression promoted Hep3B cell proliferation, migration and invasion, but hsa_circ_0008583 silencing had an opposing influence. MiR-1301-3p is directly bound to hsa_circ_0008583 and METTL3. MiR-1301-3p overexpression or METTL3 knockdown could partially counteract hsa_circ_0008583 overexpression-mediated influence on HCC cell behaviors. In addition, hsa_circ_0008583 depletion inhibits HCC tumor growth in vivo. In conclusion, hsa_circ_0008583 promotes HCC progression through the miR-1301-3p/METTL3 axis.</p

    SEM 1301(1)

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    SEM 1301(1

    ASC 1301 ORGANIC CHEMISTRY

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    ASC 1301 ORGANIC CHEMISTR

    Santa Fe (ATSF) 1301

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    A photograph print showing Santa Fe (ATSF) 1301, 4-6-2, San Bernardino, CA

    SEE 1301 ENGINEERING MATHEMATICS V

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    SEE 1301 ENGINEERING MATHEMATICS

    SEM 1301 Eng Maths V

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    SEM 1301 Eng Maths

    SEM 1301 ME14DJ Mechanics_of_Machines I

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    SEM 1301 ME14DJ Mechanics_of_Machines

    MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.

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    Chronic myeloid leukemia (CML) is a myeloproliferative disease. Imatinib (IM), the first line treatment for CML, is excessively expensive and induces various side effects in CML patients. Therefore, it is essential to investigate a new strategy for improving CML therapy. Our immunoblot data revealed that RanGTPase activating protein 1 (RanGAP1) protein levels increased by approximately 30-fold in K562 cells compared with those in normal cells. RanGAP1 is one of the important components of RanGTPase system, which regulates the export of nuclear protein. However, whether RanGAP1 level variation influences BCR-ABL nuclear export is still unknown. In this report, using shRNA to downregulate RanGAP1 expression level augmented K562 cell apoptosis by approximately 40% after treatment with 250 nM IM. Immunofluorescence assay also indicated that three-fold of nuclear BCR-ABL was detected. These data suggest that BCR-ABL nuclear entrapment induced by RanGAP1 downregulation can be used to improve IM efficacy. Moreover, our qRT-PCR data indicated a trend of inverse correlation between the RanGAP1 and microRNA (miR)-1301 levels in CML patients. MiR-1301, targeting the RanGAP1 3' untranslated region, decreased by approximately 100-fold in K562 cells compared with that in normal cells. RanGAP1 downregulation by miR-1301 transfection impairs BCR-ABL nuclear export to increase approximately 60% of cell death after treatment of 250 nM IM. This result was almost the same as treatment with 1000 nM IM alone. Furthermore, immunofluorescence assay demonstrated that Tyr-99 of nuclear P73 was phosphorylated accompanied with nuclear entrapment of BCR-ABL after transfection with RanGAP1 shRNA or miR-1301 in IM-treated K562 cells. Altogether, we demonstrated that RanGAP1 downregulation can mediate BCR-ABL nuclear entrapment to activate P73-dependent apoptosis pathway which is a novel strategy for improving current IM treatment for CML

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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