Journal: Frontiers in Pharmacology

Article Title: Berbamine sensitizes hepatocellular carcinoma to chemotherapy by inhibiting autophagy via modulating SIRT1-mediated acetylation

doi: 10.3389/fphar.2026.1763828

Figure Lengend Snippet: BBM suppresses the SIRT1-TFEB axis at the protein level. (A,B) Western blot analysis of SIRT1 and TFEB protein levels in cells treated with BBM at indicated concentrations (A) or for indicated times (B) . (C) Immunofluorescence analysis of TFEB subcellular localization. Cells were treated with BBM (5 μM) or TFEB activator 1 (0.5 μM) for 24 h and stained for TFEB (red) and DAPI (blue). Scale bar, 5 μm. (D) Intracellular NAD + levels and NAD + /NADH ratio in cells treated with BBM (2.5, 5, 10 μM) for 24 h. All values represent the mean ± SD (n = 3), * p < 0.05, ** p < 0.01. (E) Transcriptomic analysis of differentially expressed genes in SMMC-7721 cells after BBM (5 μM) treatment for 24 h. (F) Reactome pathway enrichment analysis of downregulated gene. (G) Western blot analysis of OXPHOS components (MT-ND4, MT-ND4L) in cells treated with BBM (0-10 μM) for 24 h. (H) Molecular docking analysis showing the predicted binding mode of BBM with ERRα. BBM is shown in green sticks, and hydrogen bonds are indicated as yellow dashed lines.

Article Snippet: Sorafenib (HY-10201), Baflomycin A1 (HY-100558), chloroquine (HY-17589A), rapamycin (AY-22989), resveratrol (HY-16561), and TFEB activator 1 (HY-135825) were purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Western Blot, Immunofluorescence, Staining, Binding Assay

Journal: Frontiers in Pharmacology

Article Title: Berbamine sensitizes hepatocellular carcinoma to chemotherapy by inhibiting autophagy via modulating SIRT1-mediated acetylation

doi: 10.3389/fphar.2026.1763828

Figure Lengend Snippet: SIRT1 activation rescues BBM-induced autophagy blockade. (A,B) Western blot analysis of SIRT1, TFEB, lysosomal proteins (CTSB, CTSD, RAB7), and autophagy flux markers (p62, LC3) in cells treated with BBM (5 μM) in the presence or absence of the SIRT1 agonist Resveratrol (Res, 10 μM) or the TFEB agonist TFEB activator 1 (0.5 μM) for 24 h. Data are presented as mean ± SD (n = 3). * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01 vs. BBM-only group.

Article Snippet: Sorafenib (HY-10201), Baflomycin A1 (HY-100558), chloroquine (HY-17589A), rapamycin (AY-22989), resveratrol (HY-16561), and TFEB activator 1 (HY-135825) were purchased from MedChemExpress (Princeton, NJ, USA).

Techniques: Activation Assay, Western Blot, Control

Journal: Frontiers in Neuroscience

Article Title: Deregulation of mTORC1-TFEB axis in human iPSC model of GBA1 -associated Parkinson’s disease

doi: 10.3389/fnins.2023.1152503

Figure Lengend Snippet: Decreased TFEB activity in GBA1 mutant PD neurons. Measurement of TFEB activity in: (A) WT control and GBA1 mutant PD DNCs. * p = 0.04 and *** p = 0.0003 between the indicated groups as assessed by Student’s t -test. (B) GBA1 mutant PD iPSCs and the corresponding isogenic gene-corrected line. * p = 0.03, ** p = 0.001, and *** p = 0.0002 between the indicated groups as assessed by One-way ANOVA. (C) WT control, GBA1 mutant, and gene-corrected PD DNCs. ** p = 0.009 (WT vs. PD2), ** p = 0.006 (PD2 vs. PD2 gene-corrected), ** p = 0.005 (WT vs. PD4), and ** p = 0.001 (PD4 vs. PD4 gene-corrected) as assessed by One-way ANOVA. Cells were either untreated or treated with 200 nM Torin1 for 18 h where indicated. Data represent average fold activity relative to control ± SEM, n = 3–4 per group. (D) qRT-PCR analysis showing expression of selected TFEB target genes in WT control and GBA1 mutant PD DNCs. Data represent fold relative to control ±SEM, n = 3–4 per group. **** p < 0.0001 (TFEB), * p = 0.01 (LAMP), * p = 0.04 (CTSB), ****p<0.0001 (CTSD), *** p = 0.0006 (HEXA), and ** p = 0.001 (PSAP), as assessed by Student’s t -test. (E) qRT-PCR analysis showing expression of TFEB target genes in GBA1 mutant and gene-corrected PD DNCs. Data represent fold relative to gene-corrected cells ±SEM in 2–3 independent experiments. * p = 0.03 (MCOLN), * p = 0.02 (CTSD), ** p = 0.001 (HEXA), ** p = 0.009 (CTSB), *** p = 0.0001 (PSAP), *** p = 0.0004 (LAMP,GBA), and **** p < 0.0001 (TFEB, ATP6, GNS) as assessed by Student’s t -test. (F) qRT-PCR analysis showing fold expression of TFEB target genes in GBA1 mutant and gene-corrected PD NPCs. Data represent fold relative to gene-corrected cells ±SEM in 3–4 independent experiments. ** p = 0.001 (ATP6,CTSA),** p = 0.007 (CTSD), ** p = 0.009 (MCOLN), ** p = 0.004 (LAMP,PSAP),** p = 0.001 (GBA),*** p = 0.0003 (TFEB), and **** p < 0.0001 (HEXA, GNS) as assessed by Student’s t -test. (G) qRT-PCR analysis showing expression of TFEB target genes in GBA1 mutant NPCs that were untreated or treated for 18 h with 200 nM Torin1. Data represent fold relative to untreated cells ±SEM in 2–3 independent experiments. * p = 0.04, ** p = 0.002 (CTSD), ** p = 0.009 (TFEB), *** p = 0.0003 (CLCN7), and *** p = 0.0002 (ATP6, HEXA) as assessed by Student’s t -test.

Article Snippet: TFEB transcriptional activity was measured using Human TFEB Activity Assay Kit (RayBiotech) according to the manufacturer’s instruction.

Techniques: Activity Assay, Mutagenesis, Control, Quantitative RT-PCR, Expressing