Journal: Journal of Translational Medicine

Article Title: Formyl peptide receptor 2 activation by MR-39 inhibits glioblastoma cell proliferation and invasiveness through suppression of multiple oncogenic pathways

doi: 10.1186/s12967-026-07781-3

Figure Lengend Snippet: Antiproliferative effect of MR-39 on human glioblastoma cell lines. ( A ) U87-MG, U138-MG, and U251-MG cells were exposed to 5-100 µM of MR-39 for 48 h. ( B ) Number of U87-MG, U138MG, and U251-MG cells exposed for 48 h to either the vehicle (CTRL) or 10 µM MR-39. ( C ) U87-MG, U138-MG, and U251-MG cells were exposed to either vehicle (CTRL) or 10 µM MR-39, with or without the FPR2 antagonist WRW4 (10 µM). ( D ) U87-MG cells were transfected with FPR2-targeting antisense siRNA1 or a negative control (siRNA-), followed by treatment with or without 10 µM MR-39. Cell proliferation was measured using the CCK-8 assay and is expressed as a percentage of the control. Data are expressed as means ± SEM, n = 3. Statistically significant differences are based on an unpaired t-test * p value < 0.05, ** p value < 0.005, *** p value < 0.001, **** p value < 0.0001 or one-way ANOVA followed by Tukey’s multiple comparison test

Article Snippet: EA.hy926 (CRL-2922 TM) andU87-MG (HTB-14 TM) cell lines were acquired from ATCC, while U138MG, and U251-MG were kindly provided by Prof. Generoso Luca Colucci D’Amato, University of Campania “Luigi Vanvitelli” [ ].

Techniques: Transfection, Negative Control, CCK-8 Assay, Control, Comparison

Journal: Biomolecules

Article Title: ADAR2 Protein Is Associated with Overall Survival in GBM Patients and Its Decrease Triggers the Anchorage-Independent Cell Growth Signature

doi: 10.3390/biom12081142

Figure Lengend Snippet: ADAR2 correlates with patients’ overall survival. ( a ) IHC analysis (H&E and the corresponding ADAR2 antibody staining) of two glioblastoma tissues (examples of high and low ADAR2 levels). Subpanels A and B show a representative GBM case with high ADAR2 expression; in subpanels C and D, a GBM case with low ADAR2 expression is shown; scale bar: 200 µm. ( b ) Kaplan–Meier curve comparing the survival of GBM patients (n = 39) stratified by ADAR2 levels. The red and blue lines represent low and high ADAR2 expression, respectively, following the scores indicated in Material and Methods ( p = 0.0005; HR 3.954; 95% CI from 1834 to 8525).

Article Snippet: We analyzed the endogenous ADAR2 level (mRNA and protein) in several human GBM cell lines (A172, T98G, U118MG, U87MG, LN18, and U138-MG) that show diverse abilities to give rise to a growing tumor mass if implanted in a mouse model ( www.atcc.org , accessed on 1 January 2022) ( a,b).

Techniques: Staining, Expressing

Journal: Biomolecules

Article Title: ADAR2 Protein Is Associated with Overall Survival in GBM Patients and Its Decrease Triggers the Anchorage-Independent Cell Growth Signature

doi: 10.3390/biom12081142

Figure Lengend Snippet: ADAR2 expression level and activity across GBM cell lines. ( a ) ADAR2 expression (qRT-PCR) in normal brain (fetal and adult), astrocytes, and glioblastoma cell lines (T98G, U138-MG, U87-MG, U118-MG, LN-18, and A172). Ct values were normalized to GAPDH mRNA levels. Mean ± standard deviation ( n = 3), values are representative as means ± SD, * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001. Of note, ADAR2 activity is more robust in the whole brain (either adult or fetal) because of neuronal cells, where ADAR2 is highly active. ( b ) Western blotting analysis showing the ADAR2 level in glioblastoma cell lines. No control was added as the ADAR2 level was too high. ( c ) The recoding editing index (REI) in normal astrocytes (×10), T98-G, U87-MG, U118-MG, LN-18, and A172 glioblastoma cells lines is shown. REI values were calculated as the weighted average of editing levels over all known recording sites from the highly accurate list.

Article Snippet: We analyzed the endogenous ADAR2 level (mRNA and protein) in several human GBM cell lines (A172, T98G, U118MG, U87MG, LN18, and U138-MG) that show diverse abilities to give rise to a growing tumor mass if implanted in a mouse model ( www.atcc.org , accessed on 1 January 2022) ( a,b).

Techniques: Expressing, Activity Assay, Quantitative RT-PCR, Standard Deviation, Western Blot, Control

Journal: Antioxidants

Article Title: Sinularin Induces Oxidative Stress-Mediated Apoptosis and Mitochondrial Dysfunction, and Inhibits Angiogenesis in Glioblastoma Cells

doi: 10.3390/antiox11081433

Figure Lengend Snippet: The effects of sinularin on brain cancer cell viability. ( a ) Chemical structure of sinularin. ( b ) Concentration–response curves of cell viability for GBM 8401, U87 MG, U138 MG, and T98G after 24, 48, and 72 h of sinularin treatment as well as determined IC 50 values. Each bar represents the mean ± standard error of the mean.

Article Snippet: GBM 8401 (BCRC, CVCL_B051), U87 MG (ATCC ® HTB14), T98G (ATCC ® CRL-1690), and U138 MG (ATCC ® HTB-16) were the commercial GBM cell lines of Bioresource Collection and Research Center (Hsinchu, Taiwan) or American Type Culture Collection (Manassas, VA, USA).

Techniques: Concentration Assay

Journal: Radiation Oncology (London, England)

Article Title: Integrative analysis of therapy resistance and transcriptomic profiling data in glioblastoma cells identifies sensitization vulnerabilities for combined modality radiochemotherapy

doi: 10.1186/s13014-022-02052-z

Figure Lengend Snippet: mRNA expression analysis of DNA damage response (DDR) regulator genes, and MGMT promoter methylation analysis in human GBM cell lines. A Basal mRNA expression levels of DDR regulator genes in GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG, and U251-MG as measured by qRT-PCR (ddCT method). Expression levels were normalized to a matrix of three reference genes (18S rRNA, β2-Microglobulin, and 5’-Aminolevulinate Synthase-1), and calibrated on the expression levels of astrocytes. Three replicates were analyzed per cell line. Expression values (log2-transformed) and samples were subjected to unsupervised hierarchical clustering. B Correlation of MGMT promoter methylation status and MGMT mRNA expression levels in the employed GBM cell lines as detected by methylome array and qRT-PCR, respectively. C Protein expression levels of MGMT in GBM cells as measured by western blot. Vinculin served as loading control

Article Snippet: The human GBM cell lines A172, LN18, LN229, and T98G were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA), and the human GBM cell lines U87-MG, U138-MG, and U251-MG were purchased from Cell Lines Service GmbH (CLS, Eppelheim, Germany).

Techniques: Expressing, Methylation, Quantitative RT-PCR, Transformation Assay, Western Blot

Journal: Radiation Oncology (London, England)

Article Title: Integrative analysis of therapy resistance and transcriptomic profiling data in glioblastoma cells identifies sensitization vulnerabilities for combined modality radiochemotherapy

doi: 10.1186/s13014-022-02052-z

Figure Lengend Snippet: Validation of candidate genes by targeted inhibition and clonogenic survival assays. A Clonogenic survival of A172 and U251-MG cells after single-shot IR (0–10 Gy) and ATR inhibition by AZD-6738 (0–1.0 μM, upper panel). Immunofluorescence staining of γH2AX and 53BP1 20 h after irradiation at 4 Gy ± ATR inhibition by 1 µM AZD-6738 (lower panel). γH2AX is depicted in green, 53BP1 in red, and DNA is depicted in blue. Scale bar represents 10 µm. B Clonogenic survival of A172 and U251-MG cells after single-shot IR and LIG4 inhibition by L189 (0–50 μM, upper panel). Immunofluorescence staining of γH2AX and 53BP1 20 h after irradiation at 4 Gy ± LIG4 inhibition by 50 µM L189 as performed in A (lower panel). C Clonogenic survival of A172, U138-MG, and U251-MG cells after 24 h treatment with TMZ (0–200 μM) and ATM inhibition by KU-60019 (0–1.0 μM). Super-imposed fitting functions are linear-quadratic in case of radiation experiments and logistic in case of TMZ treatment. Results of three independent experiments are depicted for each condition, and p-values were calculated by two-way ANOVAs

Article Snippet: The human GBM cell lines A172, LN18, LN229, and T98G were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA), and the human GBM cell lines U87-MG, U138-MG, and U251-MG were purchased from Cell Lines Service GmbH (CLS, Eppelheim, Germany).

Techniques: Inhibition, Immunofluorescence, Staining, Irradiation

Journal: Oncology Reports

Article Title: Long non-coding RNA NEAT1 regulates glioma cell proliferation and apoptosis by competitively binding to microRNA-324-5p and upregulating KCTD20 expression

doi: 10.3892/or.2021.8076

Figure Lengend Snippet: Expression levels of long non-coding RNA NEAT1 in glioma tissues and cell lines. (A) NEAT1 expression in LGG and HGG tissues in a TCGA dataset. (B) RT-qPCR of NEAT1 expression in 43 pairs of glioma tissues and adjacent non-tumor tissues. Data were normalized to GAPDH mRNA expression. (C) RT-qPCR of NEAT1 expression in NHAs and six glioma cell lines (U87MG, LN229, H4, U251, U118 and A172). (D) Fluorescence in situ hybridization of NEAT1 expression (upper panels) and immunohistochemical staining of Ki-67 expression (lower panels) in glioma tissues and adjacent non-tumor tissues. Scale bar, 100 µm. (E) Kaplan-Meier survival analysis of patients with glioma stratified by high (n=314) and low (n=314) tumor expression levels of NEAT1. Data were obtained from TCGA. The experiments were performed in triplicate and data are presented as the mean ± SD. *P<0.05, **P<0.01 and ***P<0.001 vs. normal astrocytes (NHA) or as indicated. NEAT1, nuclear paraspeckle assembly transcript 1; NHAs, normal human astrocytes; LGG, low-grade glioma; HGG, high-grade glioma; RT-qPCR, reverse transcription quantitative PCR; TCGA, The Cancer Genome Atlas.

Article Snippet: A total of six human glioblastoma (GBM) cell lines, including U87MG [GBM of unknown origin; American Type Culture Collection HTB-14; short-tandem repeat (STR) profiling was performed], LN229, H4, U251, U118 (derived from the U138MG astrocytoma cell line; American Type Culture Collection HTB-15; STR profiling was performed) and A172, were obtained from The Cell Bank of Type Culture Collection of The Chinese Academy of Sciences.

Techniques: Expressing, Quantitative RT-PCR, Fluorescence, In Situ Hybridization, Immunohistochemical staining, Staining, Reverse Transcription, Real-time Polymerase Chain Reaction