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Journal: Frontiers in Pharmacology
Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis
doi: 10.3389/fphar.2026.1850685
Figure Lengend Snippet: AE regulates hTERT expression and its upstream transcription factors c-Myc and E2F1 in NPC cells in a dose-dependent manner. 5–8F and C666-1 cells were treated with AE at concentrations of 0, 10, 20, and 30 μM for 48 h. (A) Protein expression levels of hTERT, c-Myc, and E2F1 were detected by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. (B) Relative mRNA expression levels of hTERT, c-Myc, and E2F1 were detected by qRT-PCR, normalized to β-actin. All data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 compared to the control group (0 μM).
Article Snippet: Primary antibodies against hTERT (Cat# HY- P81110 ), c-Myc (Cat# 67447-1-Ig), E2F1 (Cat# GB11571-100), Ki67 (Cat# GB111499-100), Cleaved Caspase-3 (Cat# GB11532-100), and
Techniques: Expressing, Western Blot, Control, Quantitative RT-PCR
Journal: Frontiers in Pharmacology
Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis
doi: 10.3389/fphar.2026.1850685
Figure Lengend Snippet: AE suppresses NPC cell viability via the c-Myc/hTERT axis. C666-1 cells were transfected with empty vector or c-Myc overexpression plasmid (c-Myc OE), followed by 48 h treatment with 20 μM AE or DMSO. (A) qPCR verification of c-Myc overexpression efficiency. c-Myc mRNA normalized to vector group; ***P < 0.001 vs. vector. (B) Western blot demonstrating AE triggers proteasome-dependent c-Myc degradation. Cells were incubated with 20 μM AE for 48 h, with 10 μM MG132 supplemented in the final 6 h β-actin served as internal reference; **P < 0.01 vs. vector, *P < 0.05 vs. AE. (C) CCK-8 cell viability rescue assay. AE significantly reduced cell viability (***P < 0.001 vs. vector). Single c-Myc OE exerted no significant impact (ns vs. vector), whereas c-Myc overexpression partially rescued AE-mediated growth suppression ( # P < 0.05 vs. AE). (D) qPCR detection of hTERT mRNA levels. AE downregulated hTERT transcription (*P < 0.05 vs. vector). c-Myc OE significantly elevated hTERT (*P < 0.05 vs. vector), and co-transfection restored hTERT expression ( # P < 0.05 vs. AE). (E) qPCR detection of endogenous c-Myc mRNA. AE decreased basal c-Myc mRNA (*P < 0.05 vs. vector); c-Myc OE markedly upregulated c-Myc transcripts (**P < 0.01 vs. vector), and ectopic c-Myc expression partially reversed AE-induced c-Myc repression ( # P < 0.05 vs. AE). All data are presented as mean ± SD, n = 3. ns, P > 0.05; *P < 0.05, **P < 0.01, ***P < 0.001 versus vector group; # P < 0.05 versus AE single treatment group.
Article Snippet: Primary antibodies against hTERT (Cat# HY- P81110 ), c-Myc (Cat# 67447-1-Ig), E2F1 (Cat# GB11571-100), Ki67 (Cat# GB111499-100), Cleaved Caspase-3 (Cat# GB11532-100), and
Techniques: Transfection, Plasmid Preparation, Over Expression, Western Blot, Incubation, CCK-8 Assay, Rescue Assay, Cotransfection, Expressing
Journal: Frontiers in Pharmacology
Article Title: Aloe-emodin inhibits nasopharyngeal carcinoma by modulating telomerase activity involving the c-Myc/E2F1 axis
doi: 10.3389/fphar.2026.1850685
Figure Lengend Snippet: Knockdown of hTERT enhances the regulatory effects of AE on hTERT, c-Myc, and E2F1 protein expression. 5–8F and C666-1 cells were treated with Control, NC (negative control siRNA), si-hTERT (hTERT knockdown), AE (20 μM), or si-hTERT + AE for 48 h. Protein expression levels of hTERT, c-Myc, and E2F1 were analyzed by Western blotting. β-actin served as the loading control. Representative blots are shown, with densitometric quantification presented as fold change relative to the control group. Data are presented as mean ± SD, n = 3. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001 vs. control group; # P < 0.05, ## P < 0.01 vs. AE group.
Article Snippet: Primary antibodies against hTERT (Cat# HY- P81110 ), c-Myc (Cat# 67447-1-Ig), E2F1 (Cat# GB11571-100), Ki67 (Cat# GB111499-100), Cleaved Caspase-3 (Cat# GB11532-100), and
Techniques: Knockdown, Expressing, Control, Negative Control, Western Blot
Journal: iScience
Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion
doi: 10.1016/j.isci.2026.116292
Figure Lengend Snippet: Sleeve gastrectomy reduces neuronal loss and pTau pathology in the hippocampus of AD mice (A) Representative Nissl staining of the hippocampus (scale bars: 200 μm) with higher-magnification views of the CA3 region (scale bars: 20 μm). (B) Western blot analysis of hippocampal Tau, phosphorylated Tau (pTau), and β-actin protein levels. (C) Quantification of surviving neurons in the hippocampal CA3 region ( n = 3 per group). (D) Ratio of pTau to total Tau based on grayscale densitometry ( n = 3 per group). Data are presented as mean ± SD. ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001 vs. WT sham group; ## p < 0.01, ### p < 0.001 vs. AD sham group.
Article Snippet:
Techniques: Staining, Western Blot
Journal: iScience
Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion
doi: 10.1016/j.isci.2026.116292
Figure Lengend Snippet: Sleeve gastrectomy activates the hippocampal ERK/CREB/BDNF signaling pathway in mice (A) Representative immunoblots of hippocampal pERK, ERK, pCREB, CREB, BDNF, and β-actin. (B) Quantitative ratio of BDNF to β-actin protein expression ( n = 3 per group). (C) pERK to total ERK ratio ( n = 3 per group). (D) pCREB to total CREB ratio ( n = 3 per group). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 vs. WT sham group; # p < 0.05, ## p < 0.01 vs. AD sham group.
Article Snippet:
Techniques: Western Blot, Expressing
Journal: iScience
Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion
doi: 10.1016/j.isci.2026.116292
Figure Lengend Snippet: GIP receptor silencing inhibits the ERK/CREB/BDNF pathway in hippocampal HT22 cells (A) Representative immunoblots of pTau, Tau, GIPR, pTrkB, TrkB, pERK, ERK, pCREB, CREB, BDNF, and β-actin (loading control) under four treatments: NC, Aβ, Aβ+GIP, and Aβ+GIP+siGIPR. (B) pTau to Tau ratio ( n = 3 per group). (C) pTrkB to TrkB ratio ( n = 3 per group). (D) pCREB to CREB ratio ( n = 3 per group). (E) pERK to ERK ratio ( n = 3 per group). (F) BDNF to β-actin ratio ( n = 3 per group). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗∗ p < 0.001 vs. NC group; # p < 0.05, ## p < 0.01 vs. Aβ group; & p < 0.05, && p < 0.01 vs. Aβ+GIP group.
Article Snippet:
Techniques: Western Blot, Control
Journal: iScience
Article Title: Sleeve gastrectomy improves cognition by enhancing central ERK/CREB/BDNF pathway through increased GIP secretion
doi: 10.1016/j.isci.2026.116292
Figure Lengend Snippet: Combined GIP and GLP-1 treatment enhances ERK/CREB/BDNF pathway activation and reduces Tau phosphorylation in HT22 cells (A) Representative immunoblots of pTau, Tau, GIPR, GLP-1R, pTrkB, TrkB, pERK, ERK, pCREB, CREB, BDNF, and β-actin under five treatment conditions: NC (negative control), Aβ, Aβ + GLP-1, Aβ + GIP, and Aβ + GLP-1 + GIP. (B) pTau/Tau ratio ( n = 3 per group). (C) GLP-1R/β-actin ratio ( n = 3 per group). (D) GIPR/β-actin ratio ( n = 3 per group). (E) pERK/ERK ratio ( n = 3 per group). (F) pCREB/CREB ratio ( n = 3 per group). (G) pTrkB/TrkB ratio ( n = 3 per group). Data represent mean ± SD; ∗ p < 0.05, ∗∗∗∗ p < 0.0001 vs. NC; # p < 0.05, ### p < 0.001 vs. Aβ; & p < 0.05 vs. Aβ + GIP group.
Article Snippet:
Techniques: Activation Assay, Phospho-proteomics, Western Blot, Negative Control
Journal: Cancer Pathogenesis and Therapy
Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target
doi: 10.1016/j.cpt.2025.08.002
Figure Lengend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
Article Snippet: Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an
Techniques: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction