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Image Search Results
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Evaluation of U-87 MG Cell Viability Following Treatment with Bifidobacterium reuteri Ab.338 SH (B.R). Glioblastoma U-87 MG cells were treated with B.R at OD600 values of 0.8, 1.0, 1.25, and 1.5 (10 µL/mL). After 24 h of exposure, cell viability was assessed using the MTT assay. Results are presented as mean ± SD from three independent biological replicates. Differences compared to untreated controls were analyzed for statistical significance (* p < 0.05, ** p < 0.01, *** p < 0.001)
Article Snippet: The
Techniques: MTT Assay
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Cytotoxic Effects of Carboplatin (C.P) on U-87 MG Cells. U-87 MG cells were treated with increasing concentrations of C.P (16.5, 18.5, 20.5, and 22.5 µg/mL) for 24 h. Viability was determined using the MTT assay. The data, derived from three independent experiments ( n = 3), are reported as mean ± SD. Statistically significant differences compared to untreated cells are indicated (* p < 0.05, ** p < 0.01, *** p < 0.001)
Article Snippet: The
Techniques: MTT Assay, Derivative Assay
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Synergistic Cytotoxicity of Carboplatin and Bifidobacterium reuteri Ab.338 SH in U-87 MG Cells. Cells were co-treated with fixed B.R (OD600 = 1.0) and varying concentrations of C.P (128, 138, 148, and 158 ng/mL). Following 24-hour incubation, cell viability was assessed via MTT assay. Data are presented as mean ± SD from three separate experiments. Significant differences relative to the control group are denoted (* p < 0.05, ** p < 0.01, *** p < 0.001)
Article Snippet: The
Techniques: Incubation, MTT Assay, Control
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Apoptosis-Related Gene Expression in U-87 MG Cells Treated with C.P + B.R at IC₅₀. Quantitative real-time PCR was performed on cells treated with the IC₅₀ dose of C.P (148 ng/mL) in combination with B.R (OD600 = 1.0) for 24 h. The analysis revealed significant upregulation of pro-apoptotic genes (Caspase-3, −8, −9, Bax, PTEN, P53, P21, IκB, and Fas), while anti-apoptotic Bcl-2 and components of the PI3K/AKT/mTOR pathway (AKT and mTOR) were significantly downregulated. Results are shown as mean ± SD from three biological replicates. Statistical comparisons to control: * p < 0.05, ** p < 0.01, *** p < 0.001
Article Snippet: The
Techniques: Gene Expression, Real-time Polymerase Chain Reaction, Control
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Schematic representation of the molecular mechanism underlying the synergistic apoptotic effects of Bifidobacterium reuteri Ab.338 SH and Carboplatin in U-87 MG cells. The combined treatment enhances apoptotic signaling through multiple pathways. Activation of Fas and upregulation of PTEN lead to Caspase-8 and Caspase-9 activation via the extrinsic pathway. Simultaneously, downregulation of AKT signaling promotes intrinsic apoptosis through sequential activation of Caspase-3 and Caspase-9 , ultimately leading to BAX activation and cell death. The co-treatment also suppresses AKT -mediated cell survival signaling and inhibits the expression of anti-apoptotic BCL-2 via P53/P21 axis modulation. Together, these molecular events contribute to enhanced apoptosis and reduced survival in glioblastoma cells. ↑ indicates upregulation; ↓ indicates downregulation
Article Snippet: The
Techniques: Activation Assay, Expressing
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Flow Cytometric Detection of Apoptosis in U-87 MG Cells Treated with C.P + B.R at IC₅₀ Concentration. U-87 MG cells were exposed to a combination of C.P (148 ng/mL) and B.R (OD600 = 1.0) for 24 h, followed by Annexin V-FITC/PI staining and flow cytometry. Representative dot plots display four distinct populations: necrotic (Q1: Annexin⁻/PI⁺), late apoptotic (Q2: Annexin⁺/PI⁺), early apoptotic (Q3: Annexin⁺/PI⁻), and viable (Q4: Annexin⁻/PI⁻). Combined treatment markedly increased both early and late apoptotic populations compared to untreated controls. Each plot is representative of three independent experiments
Article Snippet: The
Techniques: Concentration Assay, Staining, Flow Cytometry
Journal: Cancer Cell International
Article Title: Bifidobacterium enhances the antitumor efficacy of carboplatin in glioblastoma cells: targeting apoptotic and cell cycle regulatory pathways via Caspase , AKT/PTEN , and P53/P21 signaling
doi: 10.1186/s12935-025-04099-w
Figure Lengend Snippet: Quantification of Cell Death Stages in U-87 MG Cells Following Combined C.P + B.R Treatment. Bar graph displays the distribution of viable, early apoptotic, late apoptotic, and necrotic U-87 MG cells after 24-hour exposure to the IC₅₀ dose of C.P (148 ng/mL) plus B.R (OD600 = 1.0), as determined by flow cytometry. Early apoptosis increased from 0.0% (control) to 27.64%, and late apoptosis rose to 39.78%, while necrosis remained minimal. Data are expressed as mean ± SEM from three biological replicates, with statistical significance indicated (* p < 0.05), confirming apoptosis as the predominant mechanism of cytotoxicity
Article Snippet: The
Techniques: Flow Cytometry, Control