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Cyagen Biosciences
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EuroClone
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Image Search Results
Journal: Oncology Reports
Article Title: miR-1908 as a novel prognosis marker of glioma via promoting malignant phenotype and modulating SPRY4/RAF1 axis
doi: 10.3892/or.2017.6003
Figure Lengend Snippet: miR-1908 promotes glioma cell proliferation and invasion. (A and B) The expression of miR-1908 in U251 cell were affected by transfection of miR-1908 mimics or inhibitor. (C) Downregulated miR-1908 level inhibited the proliferation of U251 cells. (D) miR-1908 significantly promoted the proliferation of U251 cells by >50% at all time-points following 72 h of incubation. (E and F) Upregulated miR-1908 enhanced invasion ability of glioma cells. (G and H) miR-1908 mimics enhanced the activity of MMP-2, while miR-1908 inhibitor reduced its activity.
Article Snippet:
Techniques: Expressing, Transfection, Incubation, Activity Assay
Journal: Oncology Reports
Article Title: miR-1908 as a novel prognosis marker of glioma via promoting malignant phenotype and modulating SPRY4/RAF1 axis
doi: 10.3892/or.2017.6003
Figure Lengend Snippet: miR-1908 enhances the ability of glioma cell anti-apoptosis via regulating Bcl-2/Bax expression. (A-D) Double staining with Annexin V-FITC and PI was used to assess apoptosis in U251 cells transfected with miR-1908 mimics or inhibitor, and miR-1908 inhibitor markedly increased cell apoptosis rate. (E) Western blot analysis was performed to determine Bcl-2 and Bax protein expression in U251 cells transfected with miR-1908 mimics or inhibitor, and Bax was increased following transfection with miR-1908 inhibitor, but a marked decrease in the expression of Bcl-2. In contrast, transfection of miR-1908 mimics downregulated the expression level of Bax.
Article Snippet:
Techniques: Expressing, Double Staining, Transfection, Western Blot
Journal: Oncology Reports
Article Title: miR-1908 as a novel prognosis marker of glioma via promoting malignant phenotype and modulating SPRY4/RAF1 axis
doi: 10.3892/or.2017.6003
Figure Lengend Snippet: miR-1908 upregulates the expression level of RAF1 through targeting SPRY4. (A and B) PPI analysis of interaction genes with SPRY4, and interaction with pro-oncogene RAF1. (C and D) The expression level of RAF1 was upregulated in glioma tissue compared with normal tissue. (E) The expression level of SPRY4 was negatively correlated with RAF1 in glioma patients from TCGA KIRC database. (F and G) miR-1908 mimics were transfected into U251 cells, the relative mRNA level of SPRY4 and RAF1 were detected by qRT-PCR. (H) Upregulated miR-1908 promoted RAF1 expression via decreasing the expression of SPRY4.
Article Snippet:
Techniques: Expressing, Transfection, Quantitative RT-PCR
Journal: Nanomaterials
Article Title: Probing Internalization Effects and Biocompatibility of Ultrasmall Zirconium Metal-Organic Frameworks UiO-66 NP in U251 Glioblastoma Cancer Cells
doi: 10.3390/nano8110867
Figure Lengend Snippet: UiO-66_N internalization by U251 cells. ( A ) Not treated cells showed no fluorescence. ( B ) UiO-66_N@Acr treated cells showed fluorescence after 48 h of treatment. Fluorescent cells accounts for 97.9% of total cells.
Article Snippet: The
Techniques: Fluorescence
Journal: Nanomaterials
Article Title: Probing Internalization Effects and Biocompatibility of Ultrasmall Zirconium Metal-Organic Frameworks UiO-66 NP in U251 Glioblastoma Cancer Cells
doi: 10.3390/nano8110867
Figure Lengend Snippet: U251 cells viability by MTT assay, after 24 ( A ) and 48 ( B ) hours of incubation with UiO-66_N at various concentrations.
Article Snippet: The
Techniques: MTT Assay, Incubation
Journal: Nanomaterials
Article Title: Probing Internalization Effects and Biocompatibility of Ultrasmall Zirconium Metal-Organic Frameworks UiO-66 NP in U251 Glioblastoma Cancer Cells
doi: 10.3390/nano8110867
Figure Lengend Snippet: Flow cytometry analysis of not treated ( A , B ) or treated ( C , D ) U251 cells with UiO-66_N (30 µg/mL) for 48 h. Left panels represent dot plot of not treated ( A ) and UiO-66_N treated ( C ) live U251 cells (gated inside the dot plot). Events outside the gate of U251 cells in UiO-66_N-treated group are mostly MOF aggregates. Right panels represent propidium iodide staining showing cell cycle profiles. No significant differences between not treated ( B ) and UiO-66_N treated ( D ) cells were detected.
Article Snippet: The
Techniques: Flow Cytometry, Staining
Journal: Nanomaterials
Article Title: Probing Internalization Effects and Biocompatibility of Ultrasmall Zirconium Metal-Organic Frameworks UiO-66 NP in U251 Glioblastoma Cancer Cells
doi: 10.3390/nano8110867
Figure Lengend Snippet: UiO-66_N administration does not induce apoptosis in U251 cells. Flow cytometry analysis of not treated ( A ) or treated U251 cells with 20 ( B ) or 50 ( C ) μg/mL UiO-66_N for 48 h. Numbers inside the gates represent percentage of apoptotic U251 cells assessed by propidium iodide staining.
Article Snippet: The
Techniques: Flow Cytometry, Staining
Journal: Nanomaterials
Article Title: Probing Internalization Effects and Biocompatibility of Ultrasmall Zirconium Metal-Organic Frameworks UiO-66 NP in U251 Glioblastoma Cancer Cells
doi: 10.3390/nano8110867
Figure Lengend Snippet: UiO-66_N do not affect Akt and ERK1/2 phosphorylation in U251 glioblastoma cells. Western blots ( A ) and densitometric quantification of Akt and ERK1/2 phosphorylation levels ( B ). The cells were treated with 30 µg/mL UiO-66_N for 48 h. Blots are representative of at least three experiments. The difference in phoAkt level is not statistically significant.
Article Snippet: The
Techniques: Phospho-proteomics, Western Blot
Journal: PLoS ONE
Article Title: Cytotoxic conjugates of betulinic acid and substituted triazoles prepared by Huisgen Cycloaddition from 30-azidoderivatives
doi: 10.1371/journal.pone.0171621
Figure Lengend Snippet: Cytotoxic activities of prepared derivatives on eight tumor (including resistant) and two normal fibroblast cell lines. All other compounds prepared in this work were also tested but their activities on these 10 cell lines were higher than 50 μM which is considered inactive.
Article Snippet: The cancer cell lines were derived from T-lymphoblastic leukemia CCRF-CEM, leukemia K562 and their multiresistant counterparts expressing P-glycoprotein, MRP1 and LRP proteins (
Techniques: