1,763,356 research outputs found
Participant 506-507 Community Conversations Letter
No full textIn this letter, Participant 506-507shares their experience, as well as the experience of their partner, in receiving the COVID-19 vaccine. They share that they are thankful for being able to receive the vaccine in a center that is professional, well-organized, and courteous.New Jersey Department of Healt
DataSheet1_Overexpression of miR-506-3p reversed doxorubicin resistance in drug-resistant osteosarcoma cells.xlsx
No full textBackground and objective: Osteosarcoma is a common primary malignant tumor of bone, and doxorubicin is one of the most widely used therapeutic drugs. While the problem of doxorubicin resistance limits the long-term treatment benefits in osteosarcoma patients. The role of miRNAs and their target genes in osteosarcoma have become increasingly prominent. Currently, there is no report on miR-506-3p reversing doxorubicin resistance by targeting STAT3 in osteosarcoma. The purpose of this study was to investigate the molecular mechanism that overexpression of miR-506-3p reverses doxorubicin resistance in drug-resistant osteosarcoma cells.Methods: Doxorubicin-resistant osteosarcoma cells (U-2OS/Dox) were constructed by intermittent stepwise increasing stoichiometry. The target genes of miR-506-3p were predicted by bioinformatics approach and the targeting relationship between miR-506-3p and STAT3 was detected using dual luciferase reporter assay. U-2OS/Dox cells were treated with miR-506-3p overexpression and STAT3 silencing respectively. Then Western blot and RT-qPCR were used to detect the protein and mRNA expression levels of JAK2/STAT3 signaling pathway, drug-resistant and apoptotic associated molecules. The migration and invasion were assessed by cell scratch assay and transwell assay. The cell proliferative viability and apoptosis were investigated by CCK8 assay and flow cytometry assay.Results: U-2OS/Dox cells were successfully constructed with a 14.4-fold resistance. MiR-506-3p is directly bound to the 3′-UTR of STAT3 mRNA. Compared with U-2OS cells, the mRNA expression of miR-506-3p was reduced in U-2OS/Dox cells. Overexpression of miR-506-3p decreased the mRNA expression levels of JAK2, STAT3, MDR1/ABCB1, MRP1/ABCC1, Survivin and Bcl-2, and decreased the protein expression levels of p-JAK2, STAT3, MDR1/ABCB1, MRP1/ABCC1, Survivin and Bcl-2, and conversely increased Bax expression. It also inhibited the proliferation, migration and invasion of U-2OS/Dox cells and promoted cells apoptosis. The results of STAT3 silencing experiments in the above indicators were consistent with that of miR-506-3p overexpression.Conclusion: Overexpression of miR-506-3p could inhibit the JAK2/STAT3 pathway and the malignant biological behaviors, then further reverse doxorubicin resistance in drug-resistant osteosarcoma cells. The study reported a new molecular mechanism for reversing the resistance of osteosarcoma to doxorubicin chemotherapy and provided theoretical support for solving the clinical problems of doxorubicin resistance in osteosarcoma.</p
Resolución UNRN N° 506/2009. Otorga equivalencia. No otorgar equivalencia.
No full textFil: Universidad Nacional de Río Negro (U). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución UNRN N° 506/2009. Otorga equivalencia. No otorgar equivalencia.fals
Additional file 2 of YY1 accelerates oral squamous cell carcinoma progression through long non-coding RNA Kcnq1ot1/microRNA-506-3p/SYPL1 axis
No full textAdditional file 2: Supplementary Figure 2. Elevating miR-506-3p restrains the functions of SCC25 cells. A. RT-qPCR for determining miR-506-3p expression after up-regulating miR-506-3p; B-C. MTT assay and and colony formation assay for testing cell proliferation after up-regulating miR-506-3p; D. Flow cytometry for measuring cell apoptosis after up-regulating miR-506-3p; E-F. Transwell assay for the determination of cell migration and invasion after up-regulating miR-506-3p; * P < 0.05 compared with the mimic-NC group; Measurement data were expressed as mean ± standard deviation
Additional file 3 of The PLAGL2/MYCN/miR-506-3p interplay regulates neuroblastoma cell fate and associates with neuroblastoma progression
No full textAdditional file 3: Table S3. The predicted target sites of miR-506-3p in the 3’UTRs of PLAGL2 and CREB3L2 mRNAs
Additional file 4 of The PLAGL2/MYCN/miR-506-3p interplay regulates neuroblastoma cell fate and associates with neuroblastoma progression
No full textAdditional file 4: Table S4. Changes in mRNA expression of PLAGL2 and CREB3L2 induced by miR-506-3p mimic detected in the gene expression microarray analysis
Additional file 2 of Exosomes derived from myeloid-derived suppressor cells facilitate castration-resistant prostate cancer progression via S100A9/circMID1/miR-506-3p/MID1
No full textAdditional file 2: Figure S2. MDSC-Exo promoted DU145 cell proliferation, invasion, and migration by modulating S100A9/circMID1/miR-506-3p/MID1 signaling. (A) Relative expressions of circMID1, miR-506-3p and MID1 in DU145 cells treated with MDSC-Exo or MDSC-Exosi-S100A9. ** P < 0.01, * vs. Exo. (B) DU145 cells were transfected with si-circMID1, miR-506-3p and si-MID1, and then treated with MDSC-Exo. Cell proliferation was measured by the CCK-8 assay in the DU145 cells with different treatments. (C) DU145 cells were transfected with over-circMID1, anti-miR-506-3p and over-MID1, and then treated with MDSC-Exosi−S100A9. Cell proliferation was measured by the CCK-8 assay. (D-E) Cell migration and invasion was evaluated by Transwell assays of these DU145 cells with the indicated treatments. Scale bar, 100 μM. **, ## P < 0.01, * vs. Exo, # vs. Exosi−S100A9. All experiments were conducted at least three times
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe 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
Additional file 1 of Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway
No full textAdditional file 1: Figure S1. (A) Pearson’s correlation analysis demonstrated that YY1 was positively corrected with SNHG17. (B-C) The effects of SNHG17 overexpression on proliferation and apoptosis were shown. (D) 20 miRNAs could bind to both CTNNB1 and SNHG17. (E) RT-qPCR evaluated 20 miRNAs expressions in cells transfected with sh-SNHG17#1. (F-G) RNA pull down was used to validate the interactions of miR-506-3p with SNHG17 and CTNNB1. (H) RT-qPCR and western blot were conducted to measure CTNNB1 expression and the level of its protein β-catenin in cells transfected with NC mimics, miR-506-3p mimics, miR-506-3p mimics + pcDNA3.1, miR-506-3p mimics + pcDNA3.1/SNHG17 (Mut) or miR-506-3p mimics + pcDNA3.1/SNHG17. **P < 0.01
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