cell culture human hepatocellular carcinoma cell lines hepg2  (ATCC)

Journal: bioRxiv

Article Title: Histone succinylation directly inhibits Jumonji domain demethylases and stabilizes repressive chromatin states

doi: 10.64898/2026.05.29.728167

Figure Lengend Snippet: (A) Global histone succinylation measured by LC-MS/MS in HepG2/C3A cells following 48 hours of sodium succinate treatment. (B) Global histone succinylation in 3D cultured HepG2/C3A spheroids following 48 hours and 1 week of sodium succinate treatment. (C) Comparison of the relative abundance of succinyl-lysine residues in H3 and H4, in either treated or untreated, cultured cells (2D) or spheroids (3D). (D) Structure of the nucleosome with H3K64 residues highlighted to demonstrate solvent accessibility. (E) Abundance of succinyl-CoA in the nuclear fraction (left) and non-nuclear fraction (right) following sodium succinate treatment. (F) Total count of HepG2/C3A cells treated with 10 mM sodium succinate continuously for 48 to 144 hours, cell count taken every 48 hours. Data are shown as mean ± SEM; * p-value <0 . 05 in two-tailed Student’s t-test .

Article Snippet: The human hepatocellular carcinoma HepG2/C3A cell line was obtained from the American Type Culture Collection (ATCC, CRL-10741).

Techniques: Liquid Chromatography with Mass Spectroscopy, Cell Culture, Comparison, Solvent, Cell Characterization, Two Tailed Test

Journal: bioRxiv

Article Title: Histone succinylation directly inhibits Jumonji domain demethylases and stabilizes repressive chromatin states

doi: 10.64898/2026.05.29.728167

Figure Lengend Snippet: (A) Schematic of peptide pull-down technique used to identify potential protein interactors with histone succinylation. (B) Volcano plot of fold change and significance of enrichment of nuclear proteins from HepG2/C3A cells to a Ksu synthetic peptide vs. Kac synthetic peptide. (C) Volcano plot of fold change and significance of enrichment of bromodomain proteins to Ksu synthetic histone peptide as compared to the Kac peptide, and (D) Ksu synthetic histone peptide as compared to an unmodified peptide. (E) Volcano plot of fold change and significance of enrichment of JmjC domain demethylases to Ksu synthetic histone peptide as compared to an Kac peptide and (F) Ksu synthetic histone peptide as compared to an unmodified peptide. (G) Crystal structure (PDB 6F6D) of an unmodified histone H3 peptide in the catalytic site of KDM6B. (H) Boltz2 model of a Ksu peptide (AARK(succinyl)A) in the catalytic site of KDM6B. (I) Enrichment of JmjC-domain demethylases to the chromatin-bound proteome of HepG2/C3A cells treated with 10 mM sodium succinate for 48 hours. A -log2 p-value greater than 4 indicates significant enrichment .

Article Snippet: The human hepatocellular carcinoma HepG2/C3A cell line was obtained from the American Type Culture Collection (ATCC, CRL-10741).

Techniques:

Journal: bioRxiv

Article Title: Histone succinylation directly inhibits Jumonji domain demethylases and stabilizes repressive chromatin states

doi: 10.64898/2026.05.29.728167

Figure Lengend Snippet: (A) Known targets of JmjC domain demethylase family enzymes. (B) Relative abundance of methylation on targets of JmjC domain demethylases in HepG2/C3A cells treated with sodium succinate. (C) Relative abundance of methylation on targets of JmjC domain demethylases in HepG2/C3A 3D cells treated with sodium succinate. (D) ChIP-MS shows co-enrichment of succinylated histone peptides with H3K27me3 peptides. Data are shown as mean ± SEM; *p-value <0 . 05, **p-value <0 . 01 in two-tailed Student’s t-test .

Article Snippet: The human hepatocellular carcinoma HepG2/C3A cell line was obtained from the American Type Culture Collection (ATCC, CRL-10741).

Techniques: Methylation, Two Tailed Test

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Staining, Western Blot, Expressing, Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Inhibition, Western Blot, Expressing, Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Staining, Extraction, Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Expressing, Control

Journal: Food Chemistry: Molecular Sciences

Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

doi: 10.1016/j.fochms.2026.100387

Figure Lengend Snippet: Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

Techniques: Protein-Protein interactions, Western Blot, Expressing, Control

Journal: bioRxiv

Article Title: An LSEC-focused computational drug repurposing platform for liver fibrosis: Identification of vorinostat and other LSEC-protective candidates

doi: 10.64898/2026.05.23.727430

Figure Lengend Snippet: (A) Summary of hepatocyte-derived factors in intercellular crosstalk during NAFLD pathogenesis. (B) Asah1 floxed ( Asah1 fl/fl /WT) mice and Asah1 fl/fl / Alb Cre mice (hepatocyte-specific deletion of Asah1 ) were fed with PD for 20 weeks. Hepatic and plasma HMGB1 levels were measured by ELISA. Hepatic HMGB1 level was normalized to total protein. (C) HepG2-hepatocytes were transfected with siNC or si ASAH1 for 48 hours, followed by treatment with vehicle or a lipid mixture consisting of free FAs (300 μM; OA: PA = 2:1) and 7K (40 μM) for 24 hours. Cell lysate and supernatant HMGB1 levels were quantified by ELISA. (D) Transwell co-culture schematic. HepG2 hepatocytes were cultured in the upper chamber, transfected with siNC or siASAH1 for 48 hours. Primary LSECs were cultured separately in the lower chamber. After transfection, co-culture was initiated with FA + 7K treatment in the upper chamber and vehicle or glycyrrhizin (60 μM, HMGB1 inhibitor) in the lower chamber for 24 hours. (E) qPCR quantification (normalized to HPRT1 ) and (F) heatmap of LSEC marker expression. Mean ± SEM; n = 4. * p < 0.05, ** p < 0.01. Abbreviations: HMGB1, high mobility group box 1; HSCs, hepatic stellate cells; RAGE, receptor for advanced glycation end products; pMEK1/2, phosphorylated mitogen-activated protein kinase kinase 1/2; pERK1/2, phosphorylated extracellular signal-regulated kinase 1/2; CCl₄, carbon tetrachloride; TAA, thioacetamide; BDL, bile duct ligation; ASH, alcoholic steatohepatitis; MCD, methionine-choline-deficient; NASH, nonalcoholic steatohepatitis; Hmgb1ΔHepΔMye, hepatocyte and myeloid cell-specific HMGB1 knockout; SHH, Sonic hedgehog; IHH, Indian hedgehog; TAZ, transcriptional co-activator with PDZ-binding motif (WWTR1); TEAD, TEA domain transcription factor; OPN, osteopontin; CEBPA, CCAAT/enhancer-binding protein alpha; EVs, extracellular vesicles; PPAR-γ, peroxisome proliferator-activated receptor gamma; α-SMA, alpha-smooth muscle actin; TIMP-2, tissue inhibitor of metalloproteinase 2; VEGF-A, vascular endothelial growth factor A; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; VEGFR-2, vascular endothelial growth factor receptor 2; mAb, monoclonal antibody; VWF, von Willebrand factor; eNOS, endothelial nitric oxide synthase; ITGβ1, integrin beta 1; ITGα9β1, integrin alpha 9 beta 1; VCAM-1, vascular cell adhesion molecule 1; MoMF, monocyte-derived macrophage; CCL2, C-C motif chemokine ligand 2; RBPJ, recombination signal binding protein for immunoglobulin kappa J region; MCP-1, monocyte chemoattractant protein-1; CCR2, C-C motif chemokine receptor 2; IRE1α, inositol-requiring enzyme 1 alpha; S1P, sphingosine-1-phosphate; S1PR1, sphingosine-1-phosphate receptor 1; FOXO1, forkhead box O1; CXCL10, C-X-C motif chemokine ligand 10; MLK3, mixed lineage kinase 3; TRAIL, TNF-related apoptosis-inducing ligand; DR5, death receptor 5; RIP1, receptor-interacting protein 1; mtDNA, mitochondrial DNA; TLR9, Toll-like receptor 9; FA, fatty acid; 7K, 7-ketocholesterol; siNC, negative control siRNA; siASAH1, ASAH1 siRNA; Gly, Glycyrrhizin; HPRT1, hypoxanthine phosphoribosyltransferase; NLRP3, NLR family pyrin domain containing 3; CASP1, caspase-1; ICAM1, intercellular adhesion molecule 1; GSDMD, gasdermin D; LYVE1, lymphatic vessel endothelial hyaluronan receptor 1; KDR, kinase insert domain receptor; PLVAP, plasmalemma vesicle-associated protein; COL4A1, collagen type IV alpha 1 chain; COL4A2, collagen type IV alpha 2 chain; TGF-β, transforming growth factor beta; MMP2, matrix metallopeptidase 2; MMP9, matrix metallopeptidase 9; NOS3, nitric oxide synthase 3; ET-1, endothelin-1.

Article Snippet: Human hepatocellular carcinoma cell line HepG2 was purchased from ATCC and maintained in Eagle’s minimum essential medium (EMEM) with 10% FBS.

Techniques: Derivative Assay, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Transfection, Co-Culture Assay, Cell Culture, Marker, Expressing, Ligation, Knock-Out, Binding Assay, Negative Control

Journal: Marine Drugs

Article Title: Antidiabetic Effects of Ecklonia cava and Dieckol via DPP-IV Inhibition and Glucose Transport Regulation

doi: 10.3390/md24050174

Figure Lengend Snippet: Effects of EC-ETAC and dieckol on glucose metabolism in Insulin-Resistant HepG2 cells. ( A ) Cell viability of HepG2 cells following treatment with EC-ETAC, dieckol, and 1 mM Metformin (MF) under IRM conditions. ( B ) Relative glucose uptake expressed as a percentage of the untreated control. ( C ) Representative Western blot bands and ( D – F ) relative quantification of p-AMPK/Total AMPK, GLUT2, and PGC-1α protein levels. Insulin resistance was induced using high-dose insulin (IRM), and Metformin (MF) served as the positive control. Results are expressed as mean ± SD (n = 3). Statistical significance is indicated by * ( p < 0.05) and ** ( p < 0.001) compared to the IRM group. Data are presented as mean ± SD (n = 3). Statistical significance compared to the control is indicated by * p < 0.05, ** p < 0.001 vs. IRM group; ## p < 0.001 vs. untreated control as determined by one-way ANOVA with Dunnett’s post hoc test.

Article Snippet: Human colorectal adenocarcinoma (Caco-2) and hepatocellular carcinoma (HepG2) cell lines were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Control, Western Blot, Quantitative Proteomics, Positive Control