u118 atcc  (ATCC)

Journal: Molecular Therapy. Nucleic Acids

Article Title: miRNA675-5p inhibitor’s dual role as novel therapeutic alternative or sensitizing treatment in resistant glioma models

doi: 10.1016/j.omtn.2025.102647

Figure Lengend Snippet: miRNA657-5p inhibitor has an anti-proliferative effect mediated by HIF-1α down-regulation (A) Viability of TMZ-resistant glioma cell lines (T98, LN18, and U118) cells, assessed by means of Trypan blue exclusion test, and expressed as the percentage of viable cells compared with untreated cells after treatment with miRNA675-5p inhibitor for 18 h. ∗∗ p < 0.01 vs. scramble-treated cells. (B) ATP level in T98, LN18, and U118 cells analyzed by Cell Tox Green kit and expressed as relative fluorescence units compared with scramble-treated cells. ∗∗∗ p < 0.001 vs. control cells. (C) Gene expression analysis for BAX , BAD , and BCL-2 analyzed by real-time PCR in T98, LN18, and U118 cells after treatment with miRNA675-5p inhibitor. Data were normalized to β-ACTIN , and the ΔΔCt values were expressed as fold of induction (FOI) of the ratio between treated and scramble-treated cells. ∗ p < 0.05; ∗∗ p < 0.01 inhibitor- vs. scramble-treated cells. (D) Analysis of caspase 3/7 activity evaluated by Caspase-Glo 3/7 Assay and expressed as relative luminescent units. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 inhibitor- vs. scramble-treated cells. (E) In silico analysis of an integrative map reconstructed after the public database (The Cancer Genome Atlas Program) interrogation based on protein-protein interaction (called interactome). (F) Gene expression analysis for HIF-1α analyzed with real-time PCR in T98, LN18, and U118 cells after treatment with miRNA675-5p inhibitor. Data were normalized to β-ACTIN , and the ΔΔCt values were expressed as the FOI of the ratio between treated and scramble-treated cells. ∗∗ p < 0.01 inhibitor- vs. scramble-treated cells. (G) ELISA-based HIF-1α nuclear (black columns) and cytoplasm (gray columns) quantification after miRNA675-5p inhibitor treatment. The data are expressed as absorbance at 450 nm. ∗∗ p < 0.01 and ∗∗∗ p < 0.001 vs. control cells in nuclear vs. cytoplasmatic localization. Graphs represent mean values ± SD of three independent experiments.

Article Snippet: U251 (ICLC, Ospedale San Martino, Genova, Italy), T98, LN18 and U118 ATCC (American Type Culture Collection, Manassas, VA, USA) were maintained in RPMI1640 (U251 and T98) or DMEM High Glucose (LN18 and U118), both supplemented with 10% heat-inactivated fetal bovine serum, 100 U/mL penicillin and 100 mg/mL streptomycin, and 2 mM glutamine (all Euroclone, Milan, Italy) in a humidified atmosphere of 5% of CO 2 at 37°C.

Techniques: CellTox Assay, Fluorescence, Control, Gene Expression, Real-time Polymerase Chain Reaction, Activity Assay, Caspase-Glo Assay, In Silico, Enzyme-linked Immunosorbent Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: miRNA675-5p inhibitor’s dual role as novel therapeutic alternative or sensitizing treatment in resistant glioma models

doi: 10.1016/j.omtn.2025.102647

Figure Lengend Snippet: miRNA675-5p inhibitor effect is due to oxidative stress (A) Luminescent assay (ROS-Glo H2O2 Assay kit) was applied to measure H 2 O 2 levels in cell culture medium of different cell lines after treatment with scramble (as control)- or miRNA675-5p inhibitor. Data were expressed as relative luminescence units (RLUs) obtained by luciferase counts normalized for the amount of total proteins quantified by Bradford assay. ∗∗∗ p < 0.001 vs. control cells; # p < 0.05 U251 vs. average ROS level in T98, LN18, and U118 cells. (B) Gene expression analysis for detox-related genes ( SOD-1 and CAT-1 ) and (C) for HIF-1α-related genes ( NRF-2 , Nf-kb , and KEAP1 ) analyzed by means of Real-time PCR in all cells. Data were normalized to β-ACTIN , and the ΔΔCt values were expressed as the FOI of the ratio between treated and scramble-treated cells. ∗ p < 0.05, ∗∗ p < 0.01; ∗∗∗ p < 0.001 vs. scramble-treated cells. (D) ATP levels in U251, T98, LN18, and U118 cells after treatment with MitoTEMPO, a ROS scavenger, and inhibitor analyzed by Cell Tox Green expressed as relative fluorescence units compared with inhibitor-treated cells alone. ∗∗ p < 0.01, ∗∗∗ p < 0.001 vs. inhibitor-treated cells; ### p < 0.001 inhibitor + MitoTEMPO vs. inhibitor alone. (E) Gene expression analysis of apoptosis-related genes ( BAX , BAD , and BCL-2 ) by real-time PCR in all cells after inhibitor of inhibitor + MitoTEMPO treatment. Data were normalized to β-ACTIN , and the ΔΔCt values were expressed as the FOI of the ratio between MitoTEMPO plus inhibitor and inhibitor-treated cells. (F–H) Relative GSH (F) and GSSG (G) abundance and GSH/GSSG ratio (H) in U251 and T98 cell line in control condition vs. inhibitor-treated cells obtained by LC-MS analysis ( n = 9). ∗∗∗ p < 0.001 vs. scramble-treated cells; # p < 0.05 and ### p < 0.001 U251 scramble-treated (control) cells vs. T98 scramble-treated (control) cells. Graphs represent mean values ± SD of three independent experiments.

Article Snippet: U251 (ICLC, Ospedale San Martino, Genova, Italy), T98, LN18 and U118 ATCC (American Type Culture Collection, Manassas, VA, USA) were maintained in RPMI1640 (U251 and T98) or DMEM High Glucose (LN18 and U118), both supplemented with 10% heat-inactivated fetal bovine serum, 100 U/mL penicillin and 100 mg/mL streptomycin, and 2 mM glutamine (all Euroclone, Milan, Italy) in a humidified atmosphere of 5% of CO 2 at 37°C.

Techniques: Luminescence Assay, H2O2 Assay, Cell Culture, Control, Luciferase, Bradford Assay, Gene Expression, Real-time Polymerase Chain Reaction, CellTox Assay, Fluorescence, Liquid Chromatography with Mass Spectroscopy

Journal: Molecular Therapy. Nucleic Acids

Article Title: miRNA675-5p inhibitor’s dual role as novel therapeutic alternative or sensitizing treatment in resistant glioma models

doi: 10.1016/j.omtn.2025.102647

Figure Lengend Snippet: miRNA675-5p sensitizes resistant cells to subsequent TMZ treatment (A and B) Representative images of immunoblots (A) and quantification histograms (B) of regulatory associated protein of mtor complex 1 (RPTOR) expression. RPTOR level was assessed in U251 (left) and T98 (right) scramble (black bars) cell lines, treated with TMZ (light gray bars) miRNA675-5p inhibitor (gray bars), or inhibitor followed by TMZ treatment (dark gray bars). Mean ± SD. ∗Significant difference, ANOVA and Tukey’s test, n = 3, p < 0.05. (C) Viability of resistant glioma cell lines (T98) cells, assessed by means of Trypan blue exclusion test, and expressed as live or dead cells after miRNA675-5p inhibition and subsequent TMZ challenge, in absence or presence of the refresh period. ∗∗ p < 0.01 dead vs. live cells; ## p < 0.01 dead cells in control vs. TMZ-treated cells. (D) Cytotoxicity evaluation of the average of T98, LN18, and U118 cells analyzed by Cell Tox Green expressed as relative fluorescence units (RFUs) compared with scramble-treated cells, in absence or presence of the refresh period. (E) Gene expression analysis of apoptosis related genes ( BAX , BAD , and BCL-2 ) by real-time PCR in all cells after TMZ treatment subsequent to miRNA675-5p inhibition. Data were normalized to β-ACTIN , and the ΔΔCt values were expressed as fold of induction (FOI) of the ratio between inhibitor + TMZ- and scramble + TMZ-treated cells. ∗∗ p < 0.01, ∗∗∗ p < 0.001 of inhibitor + TMZ- vs. scramble + TMZ-treated cells. (F) Comparison of HIF-1α expression level between U251 basal level and T98 basal and treated cells. Data were normalized to β-ACTIN , and the ΔCt values were depicted in the graph. ∗∗ p < 0.01 inhibitor alone vs. inhibitor + TMZ treatment. (G) Gene expression analysis of HIF-1α and miRNA675-5p levels by real-time PCR in all cells after TMZ treatment subsequent to miRNA675-5p inhibition. Data were normalized to β-ACTIN or U6 , respectively housekeeping reference for gene and miRNA expression, and the ΔΔCt values were expressed as FOI of the ratio between inhibitor + TMZ- and scramble + TMZ-treated cells. ∗ p < 0.05, ∗∗∗ p < 0.001 inhibitor + TMZ-vs. scramble + TMZ-treated cells.

Article Snippet: U251 (ICLC, Ospedale San Martino, Genova, Italy), T98, LN18 and U118 ATCC (American Type Culture Collection, Manassas, VA, USA) were maintained in RPMI1640 (U251 and T98) or DMEM High Glucose (LN18 and U118), both supplemented with 10% heat-inactivated fetal bovine serum, 100 U/mL penicillin and 100 mg/mL streptomycin, and 2 mM glutamine (all Euroclone, Milan, Italy) in a humidified atmosphere of 5% of CO 2 at 37°C.

Techniques: Western Blot, Expressing, Inhibition, Control, CellTox Assay, Fluorescence, Gene Expression, Real-time Polymerase Chain Reaction, Comparison

Journal: EMBO Molecular Medicine

Article Title: Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy

doi: 10.1038/s44321-025-00201-x

Figure Lengend Snippet: ( A ) Representative images of SA-β-gal staining of GBM cell lines mock-irradiated (Mock) or irradiated (IR) with 10 Gy of X-rays and then allowed to recover for 10 days ( n = 3 with at least 100 nuclei scored for each replicate). Nuclei are stained with DAPI (blue). Plots show mean percentage of SA-β-gal-positive cells +/− SD. A two-tailed Student’s t test was performed; LN229 P = 0.000009, A172 P = 0.000027, U118 P = 0.000141, U87 P = 0.007801. Scale bar, 100 μm. ( B ) Whole cell extracts from mock-irradiated or irradiated GBM cell lines were western blotted with anti-p21 antibody. Actin serves as loading control. ( C ) Volcano plot representation of differentially expressed genes from mock-irradiated vs . irradiated LN229 or A172 cells ( n = 3), as assessed by RNA sequencing 10 days after treatment with 10 Gy of X-rays. Differential gene expression analysis was performed using edgeR. Gene-specific dispersions were estimated using a tagwise dispersion model and statistical significance was assessed using the likelihood ratio test (LRT). The false discovery rate (FDR) was calculated using the Benjamini–Hochberg procedure. Genes with an FDR < 0.05 with log 2 fold change (Log 2 FC) cutoff of −1 and 1 were considered differentially expressed, as denoted by dashed lines. Core SASP genes that were further validated by qRT-PCR are represented by numbers. ( D ) Total RNA was isolated from GBM cells 10 days after irradiation with 10 Gy of X-rays or from mock-irradiated cells and expression of SASP genes assessed by qRT-PCR ( n = 3 biological replicates comprising three technical replicates each). Plots show mean fold change (Log 2 FC) in gene expression +/− SD of SASP-related genes in irradiated GBM cells relative to mock-irradiated cells. A two-tailed Student’s t test was performed; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001 (please refer to Appendix Table for the exact p values). ( E ) Conditioned media were collected from GBM cells 10 days after irradiation with 10 Gy of X-rays ( n = 3 biological replicates comprising three technical replicates each), and cytokine levels were measured by multiplex bead-based immunoassay. Plots show mean fold change (Log 2 FC) in cytokine levels +/− SD in media from irradiated cells relative to mock-irradiated cells. A two-tailed Student’s t test was performed; ** P < 0.01; *** P < 0.001; **** P < 0.0001 (please refer to Appendix Table for the exact P values). .

Article Snippet: U118 , ATCC , HTB-15.

Techniques: Staining, Irradiation, Two Tailed Test, Western Blot, Control, RNA Sequencing, Gene Expression, Dispersion, Quantitative RT-PCR, Isolation, Expressing, Multiplex Assay, Bead-based Assay

Journal: EMBO Molecular Medicine

Article Title: Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy

doi: 10.1038/s44321-025-00201-x

Figure Lengend Snippet: ( A ) Representative images of GBM cell lines immunofluorescence stained for Lamin B1 (green) and ( B ) Ki67 (green), 10 days after irradiation (IR) with 10 Gy of X-rays or mock-irradiation (Mock). n = 3 with at least 100 nuclei scored for each replicate. Nuclei are stained with DAPI (blue). Plots show mean percentages +/− SD of Lamin B1- or Ki67-positive cells. A two-tailed Student’s t test was performed; Lamin B1 - LN229 P = 0.00000163109, A172 P = 0.00000004724, U118 P = 0.00000000002, U87 P = 0.00000702223; Ki67 - LN229 P = 0.000030, A172 p = 0.000002, U118 p = 0.000028, U87 P = 0.000005. Scale bar, 50 μm. ( C ) Heatmap of top 100 differentially expressed genes in LN229 or A172 GBM cells mock-irradiated (Mock) or irradiated (IR) with 10 Gy of X-rays and then allowed to recover for 10 days ( n = 3), as assessed by RNA sequencing. ( D ) Senescence scores of mock-irradiated or irradiated LN229 and A172 cells ( n = 3) generated by analysis of RNA-seq datasets using the SenCan Classifier tool. Score ranges from 0 (no senescence) to 1 (senescence). Plot shows mean senescence score +/− SD for both GBM cell lines. A two-tailed Student’s t test was performed; LN229 P = 0.00002368169637, A172 p = 0.00000000000002. ( E ) Genes involved in SASP, Cytokine-cytokine receptor interaction, JAK-STAT signaling, and NF-kB signaling are significantly enriched in irradiated cells compared to mock-irradiated cells. Normalized Enrichment Scores (NES) are shown in the figure; P = 0. ( F ) SASP-transcription factor network generated by the list of 24 common cytokines secreted by all four senescent GBM cell lines cross-referenced against the TRRUST database. The visualization was generated using Cytoscape version 3.9.1. Transcription factors are shown in green. The cytokines not shown had no available information in the database. .

Article Snippet: U118 , ATCC , HTB-15.

Techniques: Immunofluorescence, Staining, Irradiation, Two Tailed Test, RNA Sequencing, Generated

Journal: EMBO Molecular Medicine

Article Title: Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy

doi: 10.1038/s44321-025-00201-x

Figure Lengend Snippet: ( A ) Naive GBM cells were exposed to conditioned media from senescent (CM-SEN) or non-senescent (CM-NS) GBM cells for the indicated times, and activation of the JAK-STAT3 pathway assessed by western blotting with anti-phopho-STAT3 (Y705) antibody. Actin serves as loading control. Recipient cells were serum starved (ss) before addition of CM. ( B ) Phosphorylation of STAT3 after exposure of naive cells to CM-SEN for 30 min was assessed by western blotting after either neutralization of IL-6 in the conditioned media with an anti-IL-6 antibody (N-α-IL-6) or treatment of recipient GBM cells with the JAK inhibitor ruxolitinib, as indicated. ( C ) Serum starved (ss) GBM cells were pulsed with BrdU after exposure to CM-NS, CM-SEN, or CM-SEN in the presence of ruxolitinib (CM-SEN+Ruxo), and immunofluorescence stained with anti-BrdU antibody (red), as indicated ( n = 3 with at least 100 nuclei scored for each replicate). Nuclei are stained with DAPI (blue). Plots show mean percentages of BrdU-positive cells +/− SD. A two-tailed Student’s t test was performed; LN229 P = 0.00183, 0.0028; A172 P = 0.01061, 0.03826; U118 P = 0.00736, 0.02480; U87 P = 0.00002, 0.00002, respectively. Scale bar, 10 μm. .

Article Snippet: U118 , ATCC , HTB-15.

Techniques: Activation Assay, Western Blot, Control, Phospho-proteomics, Neutralization, Immunofluorescence, Staining, Two Tailed Test

Journal: EMBO Molecular Medicine

Article Title: Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy

doi: 10.1038/s44321-025-00201-x

Figure Lengend Snippet: ( A ) Kaplan–Meier curve showing lack of correlation of Bcl2l10 expression levels with prognosis in GBMLGG patients in TCGA ( n = 606) and CGGA ( n = 657) cohorts as evidenced by Hazard Ratio (logrank) of 0.9692 and 0.8629 and P values of 0.1943 and 0.2640, respectively. ( B ) Plot shows mean relative expression of BIRC2 + /− SD in mock-irradiated vs. irradiated (IR) GBM cells 10 days after exposure to 10 Gy of X-rays, as assessed by qRT-PCR ( n = 3 biological replicates comprising 3 technical replicates each). A two-tailed Student’s t test was performed; exact P values from left to right: 0.0000001, 0.0010112, 0.0044335, 0.9295618. ( C ) Whole cell extracts from mock-irradiated or irradiated GBM cell lines were western blotted with anti-cIAP1 antibody. Actin serves as loading control. ( D ) Senescent GBM cells (10 days after exposure to 10 Gy) were treated with the IKK inhibitor BMS-345541 (BMS) or DMSO as control for 72 h ( n = 3 biological replicates comprising 3 technical replicates each), and mean relative expression of BIRC3 + /− SD was assessed by qRT-PCR (a two-tailed Student’s t test was performed; A172 p = 0.00000003, 0.00000232; U118 p = 0.00000220, 0.00026887; U87 P = 0.00000818, 0.00118914, respectively) or ( E ) western blotting for cIAP2. ( F ) Naive GBM cells were exposed to conditioned media from senescent (CM-SEN) or non-senescent (CM-NS) cells for the indicated times, and expression of cIAP2 assessed by western blotting. ( G ) Naive GBM cells were treated with BMS-345541 or DMSO as control for 2 h before exposure to CM-SEN ( n = 3 biological replicates comprising 3 technical replicates each), and mean relative expression of BIRC3 + /− SD was assessed by qRT-PCR (a two-tailed Student’s t test was performed; A172 P = 0.000627, 0.000622; U118 P = 0.000001, 0.000001; U87 P = 0.000593, 0.000936, respectively) or ( H ) western blotting for cIAP2. ( I ) GBM cells were exposed to conditioned media from senescent or non-senescent cells ( n = 3) and radiation sensitivity measured by the colony survival assay. The mean percentage of surviving colonies +/− SD ( y axis) is plotted against the corresponding radiation dose ( x axis). .

Article Snippet: U118 , ATCC , HTB-15.

Techniques: Expressing, Irradiation, Quantitative RT-PCR, Two Tailed Test, Western Blot, Control, Clonogenic Cell Survival Assay

Journal: EMBO Molecular Medicine

Article Title: Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy

doi: 10.1038/s44321-025-00201-x

Figure Lengend Snippet: Reagents and tools table

Article Snippet: U118 , ATCC , HTB-15.

Techniques: Biomarker Discovery, Purification, Sequencing, Negative Control, Plasmid Preparation, Fluorsave, SYBR Green Assay, Western Blot, Stripping, Software

Journal: Marine Drugs

Article Title: The Marine-Derived Macrolactone Mandelalide A Is an Indirect Activator of AMPK

doi: 10.3390/md20070418

Figure Lengend Snippet: Mandelalide L induces time and concentration-dependent phosphorylation of AMPK and ACC. ( A ) Immunoblot analysis of U87-MG glioblastoma cells treated with mandelalide A for 30 min. Whole cell lysates were probed with antibodies for phospho-AMPK, phospho-ACC, total AMPK, total ACC and GAPDH as indicated. Blots are representative of a single experiment that was repeated three times. ( B ) Histograms show quantification of immunoblot data shown in A from three independent experiments; phospho-AMPK/total AMPK and phospho-ACC/total ACC, normalized to loading control ( C ) Immunoblot analysis of U87-MG treated with 1 μM of mandelalide L for 30 min, 1 h or 4 h and probed with antibodies shown in A. ( D ) Histograms show the quantification of immunoblot data shown in C from three independent experiments; phospho-AMPK/total AMPK and phospho-ACC/total ACC, normalized to loading control. Statistical significance of change relative to vehicle (0.1% DMSO) is indicated in B and D as * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human U87-MG glioblastoma, U118 glioblastoma, HeLa cervical, H292, A549 and H3122 lung cancer cells were from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Concentration Assay, Phospho-proteomics, Western Blot, Control

Journal: Marine Drugs

Article Title: The Marine-Derived Macrolactone Mandelalide A Is an Indirect Activator of AMPK

doi: 10.3390/md20070418

Figure Lengend Snippet: Comparative analysis of mandelalide A-induced changes in growth and AMPK signaling in human HeLa cervical and U87-MG glioblastoma cells. ( A ) Concentration-dependent changes in the growth of human HeLa cells and U87-MG glioblastoma cells in response to mandelalide A or vehicle (0.1% DMSO). Antiproliferative effects were calculated using an MTT antiproliferative/viability assay with the viability of vehicle-treated cells defined as 100%. Cells were either untreated (time zero) or exposed to treatment for 72 h. Cell density at the time of treatment is indicated by a dashed black line at 0% growth. Graphs represent mean viability ± S.E. ( n = 3 wells per treatment) and curves represent the fit of data points by nonlinear regression analysis to a logistic equation. Curves represent the fit of data from at least three independent comparisons. ( B ) Immunoblot analysis of AMPK and ACC status in HeLa cervical and U87-MG glioblastoma cells treated with (+) mandelalide A (30 nM or 100 nM) or (−) vehicle (0.1% DMSO) for 30 min or 90 min. Whole cell lysates were collected, processed for western blot and probed with primary antibodies against phospho-AMPK, phospho-ACC, total AMPK, total ACC, LKB1 and GAPDH as indicated. ( C ) Histograms show the quantification of phospho-AMPK/total AMPK and phospho-ACC/total ACC normalized to GAPDH from three independent experiments. Statistical significance of change relative to vehicle (0.1% DMSO) is indicated as * p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: Human U87-MG glioblastoma, U118 glioblastoma, HeLa cervical, H292, A549 and H3122 lung cancer cells were from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Concentration Assay, Viability Assay, Western Blot

Journal: Marine Drugs

Article Title: The Marine-Derived Macrolactone Mandelalide A Is an Indirect Activator of AMPK

doi: 10.3390/md20070418

Figure Lengend Snippet: Mandelalide A is a potent and efficacious cytotoxin to human glioblastoma cells. Concentration-response relationships for ( A , B ) mandelalide A- or ( C , D ) erlotinib-induced toxicity to human U87-MG, U251, F-295, SF268 and U118 glioblastoma cells. Cells were continuously exposed to test compound or vehicle (0.1% DMSO) for three days ( A , C ) or six (three + three) days ( B , D ). Cell viability was assessed using a CellTiter-Glo ® assay with the viability of vehicle-treated control cells defined as 100%. A single concentration of salinosporamide A (SLA; 1 µM) was used as a positive cytotoxic control. Graphs represent mean viability ±S.E. ( n = three wells per treatment) and curves represent the fit of data points by nonlinear regression analysis to a logistic equation. Curves represent the fit of data from at least three independent comparisons.

Article Snippet: Human U87-MG glioblastoma, U118 glioblastoma, HeLa cervical, H292, A549 and H3122 lung cancer cells were from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Concentration Assay, Glo Assay, Control

Journal: Marine Drugs

Article Title: The Marine-Derived Macrolactone Mandelalide A Is an Indirect Activator of AMPK

doi: 10.3390/md20070418

Figure Lengend Snippet: Comparative analysis of the cytotoxic potential of mandelalide A or erlotinib to a panel of human glioblastoma cells.

Article Snippet: Human U87-MG glioblastoma, U118 glioblastoma, HeLa cervical, H292, A549 and H3122 lung cancer cells were from the American Type Culture Collection (Manassas, VA, USA).

Techniques:

Journal: PLoS ONE

Article Title: Assessment of the proliferation status of glioblastoma cell and tumour tissue after nanoplatinum treatment

doi: 10.1371/journal.pone.0178277

Figure Lengend Snippet: Optical microscopy images of platinum nanoparticles (NP-Pt) or cisplatin -treated and untreated U87 and U118 glioma cells. (A) U87 control; (B) NP-Pt—treated U87; (C) cisplatin-treated U87; (D) U118 control; (E) NP-Pt-treated U118; (F) cisplatin-treated U118. BrdU incorporation assay–(G)–U87 cells; (H)–U188 cells. a, b Values with different letters are significantly different, P < 0.05. Bar scale 100μm.

Article Snippet: Human glioblastoma U118 and glioblastoma likely U87 cell [ , ] lines were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in Dulbecco’s modified Eagle’s culture medium supplemented with 10% foetal bovine serum (Sigma-Aldrich), 1% penicillin, and streptomycin (Sigma-Aldrich) at 37°C in a humidified atmosphere of 5% CO2/95% air in a NuAire DH AutoFlow CO2 Air-Jacketed Incubator (Plymouth, MN, USA).

Techniques: Microscopy, Control, BrdU Incorporation Assay

Journal: PLoS ONE

Article Title: Assessment of the proliferation status of glioblastoma cell and tumour tissue after nanoplatinum treatment

doi: 10.1371/journal.pone.0178277

Figure Lengend Snippet: Numbers of PCNA positive nuclei in glioblastoma multiforme tumour tissue (area counted 3500 μm 2 ) in the control group and in groups treated with platinum nanoparticles and cisplatin.

Article Snippet: Human glioblastoma U118 and glioblastoma likely U87 cell [ , ] lines were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in Dulbecco’s modified Eagle’s culture medium supplemented with 10% foetal bovine serum (Sigma-Aldrich), 1% penicillin, and streptomycin (Sigma-Aldrich) at 37°C in a humidified atmosphere of 5% CO2/95% air in a NuAire DH AutoFlow CO2 Air-Jacketed Incubator (Plymouth, MN, USA).

Techniques: Control

Journal: PLoS ONE

Article Title: Assessment of the proliferation status of glioblastoma cell and tumour tissue after nanoplatinum treatment

doi: 10.1371/journal.pone.0178277

Figure Lengend Snippet: Visualization of PCNA via immunohistochemistry (A, B, C) and immunofluorescence (D, E, F, G, H, I) in glioblastoma tumours. (A), (D), (G)- U87 control; (B), (E), (H)- NP-Pt—treated U87; (C), (F), (I)- cisplatin-treated U87. Scale bars: 50 μm. Note: white arrows point to PCNA positive nuclei.

Article Snippet: Human glioblastoma U118 and glioblastoma likely U87 cell [ , ] lines were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in Dulbecco’s modified Eagle’s culture medium supplemented with 10% foetal bovine serum (Sigma-Aldrich), 1% penicillin, and streptomycin (Sigma-Aldrich) at 37°C in a humidified atmosphere of 5% CO2/95% air in a NuAire DH AutoFlow CO2 Air-Jacketed Incubator (Plymouth, MN, USA).

Techniques: Immunohistochemistry, Immunofluorescence, Control