cell culture human hepatocellular carcinoma cell lines hepg2  (ATCC)

Journal: Journal of Oral Microbiology

Article Title: Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis -induced proliferation in liver cancer cells

doi: 10.1080/20002297.2026.2684127

Figure Lengend Snippet: Effects of Pg on cell proliferation. The proliferation of pancreatic cancer cells (a) and HepG2 cells (b) treated with varying multiplicities of infection (MOI) of Pg was measured using cell viability assays as described in the Methods. (c) Data are expressed as the mean ± SD ( n = 3). *, p < 0.05; **, p < 0.01 vs. control (MOI 0). One-way ANOVA with Dunnett's post hoc test was used.

Article Snippet: HepG2 hepatocellular carcinoma cells (ATCC, Manassas, VA, USA), along with control cells such as human pancreatic carcinoma cells (RCB 1973: PK-45H, RIKEN BRC, Japan) and HuH7 liver cancer cells (ATCC, Manassas, VA, USA), were used in this study.

Techniques: Infection, Control

Journal: Journal of Oral Microbiology

Article Title: Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis -induced proliferation in liver cancer cells

doi: 10.1080/20002297.2026.2684127

Figure Lengend Snippet: Activation of TLR, ERK, Akt and NF-κB signaling pathways in response to Pg treatment. Western blot analysis of the protein levels of TLR4, p -ERK, p -Akt and p -NF-κB in pancreatic cancer cells and HepG2 cells treated with Pg is shown. The total protein level of the respective protein was blotted as the internal control. The ratios of arbitrary values of protein levels of TLR4 (a, e), p -ERK (b, f), p -Akt (c, g) and p -NF-κB (d, h) against the internal control are shown right under the respective western blotting bands. Data are expressed as the mean ± SD ( n = 3). Tukey's post hoc test was used.

Article Snippet: HepG2 hepatocellular carcinoma cells (ATCC, Manassas, VA, USA), along with control cells such as human pancreatic carcinoma cells (RCB 1973: PK-45H, RIKEN BRC, Japan) and HuH7 liver cancer cells (ATCC, Manassas, VA, USA), were used in this study.

Techniques: Activation Assay, Protein-Protein interactions, Western Blot, Control

Journal: Journal of Oral Microbiology

Article Title: Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis -induced proliferation in liver cancer cells

doi: 10.1080/20002297.2026.2684127

Figure Lengend Snippet: Effects of LPS derived from Pg and CA on cell proliferation. Proliferation of pancreatic cancer cells (a) and HepG2 cells (b) treated with 1 µg/mL Pg-derived LPS alone and in combination with 10 µM CA was detected as described in the Methods. Data are expressed as the mean ± SD ( n = 3). *, p < 0.05 vs. control. **, p < 0.01 vs. control. Tukey's post hoc test was used.

Article Snippet: HepG2 hepatocellular carcinoma cells (ATCC, Manassas, VA, USA), along with control cells such as human pancreatic carcinoma cells (RCB 1973: PK-45H, RIKEN BRC, Japan) and HuH7 liver cancer cells (ATCC, Manassas, VA, USA), were used in this study.

Techniques: Derivative Assay, Control

Journal: Journal of Oral Microbiology

Article Title: Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis -induced proliferation in liver cancer cells

doi: 10.1080/20002297.2026.2684127

Figure Lengend Snippet: Differential effects of CA on HepG2 and HuH7 cell proliferation: cell type dependency. (a) Proliferation of HuH7 cells stimulated with Pg at the indicated MOI and (b) proliferation of HuH7 cells under four conditions (control, LPS, LPS + CA and CA alone). (c) Proliferation of HuH7 cells and (d) HepG2 cells treated with CA at concentrations ranging from 0.1 µM to 10 µM. All proliferation assays were performed as described in the Methods. Data are expressed as mean ± SD ( n = 3). *, p < 0.05; **, p < 0.01 vs. control. One-way ANOVA with Dunnett's post hoc test was used for (a), (c) and (d). Tukey's post hoc test was used for (b).

Article Snippet: HepG2 hepatocellular carcinoma cells (ATCC, Manassas, VA, USA), along with control cells such as human pancreatic carcinoma cells (RCB 1973: PK-45H, RIKEN BRC, Japan) and HuH7 liver cancer cells (ATCC, Manassas, VA, USA), were used in this study.

Techniques: Control

Journal: Journal of Oral Microbiology

Article Title: Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis -induced proliferation in liver cancer cells

doi: 10.1080/20002297.2026.2684127

Figure Lengend Snippet: Nrf2 nuclear translocation in response to CA treatment. Immunofluorescence staining of HuH7 cells (a) and HepG2 cells (c) treated with 10 µM CA, showing Nrf2 (red) and nuclei (blue). Overlap indicates Nrf2 translocation to the nucleus. Quantification of cells with nuclear Nrf2 (%) is shown in (b) and (d). Data are mean ± SD ( n = 3). ** p < 0.01 vs. control. Unpaired two-tailed Student's t-test was used.

Article Snippet: HepG2 hepatocellular carcinoma cells (ATCC, Manassas, VA, USA), along with control cells such as human pancreatic carcinoma cells (RCB 1973: PK-45H, RIKEN BRC, Japan) and HuH7 liver cancer cells (ATCC, Manassas, VA, USA), were used in this study.

Techniques: Translocation Assay, Immunofluorescence, Staining, Control, 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) 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