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human intestinal epithelial cell line fhc (ATCC)

Name: human intestinal epithelial cell line fhc
Brand: ATCC
Rating: 97 (963 reviews)

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ATCC human intestinal epithelial cell line fhc

IRX4 Expression is Significantly Downregulated in CRC. (A, B) Immunofluorescence staining of IRX4 (red) and the cell nucleus (blue), showing that IRX4 is primarily localized in the nucleus, with significantly reduced average fluorescence intensity in CRC cells compared to normal <t>intestinal</t> <t>epithelial</t> cells. Scale bar: 50 μm. (C, D) Protein expression of IRX4 in CRC tissues and adjacent normal tissues with statistical analysis. (E, F) Proin expression of IRX4 in CRC cells and normal intestinal epithelial cells. (G) RT-qPCR analysis of IRX4 expression in CRC tissues and corresponding adjacent normal tissues. (H) mRNA expression of IRX4 in four CRC cell lines compared to <t>FHC</t> cells. Data are presented as the mean ± SEM (n = 3). P < 0.05 is considered the difference to be statistically significant.

Human Intestinal Epithelial Cell Line Fhc, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 963 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Anti-colorectal cancer effects of IRX4 and sensitivity studies to oxaliplatin"

Article Title: Anti-colorectal cancer effects of IRX4 and sensitivity studies to oxaliplatin

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2025.1581244

Figure Legend Snippet: IRX4 Expression is Significantly Downregulated in CRC. (A, B) Immunofluorescence staining of IRX4 (red) and the cell nucleus (blue), showing that IRX4 is primarily localized in the nucleus, with significantly reduced average fluorescence intensity in CRC cells compared to normal intestinal epithelial cells. Scale bar: 50 μm. (C, D) Protein expression of IRX4 in CRC tissues and adjacent normal tissues with statistical analysis. (E, F) Proin expression of IRX4 in CRC cells and normal intestinal epithelial cells. (G) RT-qPCR analysis of IRX4 expression in CRC tissues and corresponding adjacent normal tissues. (H) mRNA expression of IRX4 in four CRC cell lines compared to FHC cells. Data are presented as the mean ± SEM (n = 3). P < 0.05 is considered the difference to be statistically significant.

Techniques Used: Expressing, Immunofluorescence, Staining, Fluorescence, Quantitative RT-PCR

Image Search Results

Cytotoxicity and inhibitory effects on RV replication of different HSP90 inhibitors. ( A ) Plots for cell viability of MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. Cell viability was tested using the CCK-8 assay. ( B ) Plots for RV (Wa and SA11 strains) inhibition in MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. RV replication was tested by PFA, and IC 50 values are indicated at the top of each plot. The experiments were performed in triplicate, and the data are presented as mean ± SEM and are representative of four ( A ) and two ( B ) independent experiments. ns, not significant; * P < 0.05, ** P < 0.01, **** P < 0.0001 (two-way ANOVA).

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: Cytotoxicity and inhibitory effects on RV replication of different HSP90 inhibitors. ( A ) Plots for cell viability of MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. Cell viability was tested using the CCK-8 assay. ( B ) Plots for RV (Wa and SA11 strains) inhibition in MA104, Caco-2, and HT-29 cells after treatment with NVP-HSP990, GA, or 17-AAG at indicated concentrations for 24 h. RV replication was tested by PFA, and IC 50 values are indicated at the top of each plot. The experiments were performed in triplicate, and the data are presented as mean ± SEM and are representative of four ( A ) and two ( B ) independent experiments. ns, not significant; * P < 0.05, ** P < 0.01, **** P < 0.0001 (two-way ANOVA).

Article Snippet: Human intestinal epithelial cell lines Caco-2 cells (ATCC: HTB-37) and HT-29 cells (ATCC: HTB-38) were from ATCC and kept in our institute.

Techniques: CCK-8 Assay, Inhibition

NVP-HSP990 significantly inhibited RV replication, viral gene transcription, and antigen expression. ( A ) Caco-2 cells were infected with RV (Wa or SA11 strains) at varying MOIs (0.001–10), followed by treatment with 100 nM NVP-HSP990 or an equal volume of DMSO (as a control) for 24 h. Viral replication was assessed using PFA. ( B ) Schematic diagram illustrating the timing of NVP-HSP990 addition and removal. ( C ) Caco-2 cells were infected with RV (MOI = 1) and treated with 100 nM NVP-HSP990 or with DMSO as control at indicated infection periods as shown in panel B. Viral replication was tested with PFA at 20 h p.i. ( D ) Caco-2 cells were infected with RV (MOI = 1) and treated with 100 nM HSP990 at 0, 4, 8, 12 h p.i. or treated with DMSO at 0 h p.i. Virus replication was tested with PFA at 24 h p.i. ( E ) Caco-2 cells were infected with RV (MOI = 1) and further cultivated with DMEM containing 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the infected cells were harvested for qPCR analysis of the expression of RV genes encoding the VP2, VP6, NSP4, and NSP5 proteins. ( F ) Caco-2 cells were mock-infected with PBS or infected with RV (MOI = 1) and further cultivated with DMEM containing 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the cells were harvested for WB analysis of RV structural proteins VP6 and VP7. ( G ) Caco-2 cells growing on coverslips were mock-infected with PBS or infected with RV (MOI = 3) and treated with 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the infected cells were subjected to immunostaining of RV VP6 antigens (red). Data are presented as mean ± SEM ( A, C, D, E ). The experiments were performed in triplicate ( A, C, D, E ), and the data are representative of two independent experiments ( A, C–G ). ns, not significant; ** P < 0.01, *** P < 0.001, **** P < 0.0001 (two-way ANOVA [ A, C, E ] and one-way ANOVA [ D ]).

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: NVP-HSP990 significantly inhibited RV replication, viral gene transcription, and antigen expression. ( A ) Caco-2 cells were infected with RV (Wa or SA11 strains) at varying MOIs (0.001–10), followed by treatment with 100 nM NVP-HSP990 or an equal volume of DMSO (as a control) for 24 h. Viral replication was assessed using PFA. ( B ) Schematic diagram illustrating the timing of NVP-HSP990 addition and removal. ( C ) Caco-2 cells were infected with RV (MOI = 1) and treated with 100 nM NVP-HSP990 or with DMSO as control at indicated infection periods as shown in panel B. Viral replication was tested with PFA at 20 h p.i. ( D ) Caco-2 cells were infected with RV (MOI = 1) and treated with 100 nM HSP990 at 0, 4, 8, 12 h p.i. or treated with DMSO at 0 h p.i. Virus replication was tested with PFA at 24 h p.i. ( E ) Caco-2 cells were infected with RV (MOI = 1) and further cultivated with DMEM containing 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the infected cells were harvested for qPCR analysis of the expression of RV genes encoding the VP2, VP6, NSP4, and NSP5 proteins. ( F ) Caco-2 cells were mock-infected with PBS or infected with RV (MOI = 1) and further cultivated with DMEM containing 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the cells were harvested for WB analysis of RV structural proteins VP6 and VP7. ( G ) Caco-2 cells growing on coverslips were mock-infected with PBS or infected with RV (MOI = 3) and treated with 100 nM NVP-HSP990 or DMSO as control for 18 h. Then the infected cells were subjected to immunostaining of RV VP6 antigens (red). Data are presented as mean ± SEM ( A, C, D, E ). The experiments were performed in triplicate ( A, C, D, E ), and the data are representative of two independent experiments ( A, C–G ). ns, not significant; ** P < 0.01, *** P < 0.001, **** P < 0.0001 (two-way ANOVA [ A, C, E ] and one-way ANOVA [ D ]).

Article Snippet: Human intestinal epithelial cell lines Caco-2 cells (ATCC: HTB-37) and HT-29 cells (ATCC: HTB-38) were from ATCC and kept in our institute.

Techniques: Expressing, Infection, Control, Virus, Immunostaining

NVP-HSP990 alters the life state of host cells. Caco-2 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3) and further cultivated with DMEM containing 100 nM NVP-HSP990 or an equal volume of DMSO as a control for 24 h. Then, the infected cells were harvested for RNA-seq analysis. ( A ) Multiple differential scatter plots of compared groups. ( B ) Venn diagrams of up- and downregulated genes between compared groups. ( C, D ) Top 10 (ranked by descending Q value) upregulated ( C ) and downregulated ( D ) KEGG pathways in all mock-, Wa-, and SA11-infected Caco-2 cells. ( E, F ) Top 10 (ranked by descending Q value) upregulated ( E ) and downregulated ( F ) KEGG pathways in both Wa- and SA11-infected but not in mock-infected Caco-2 cells. *Q value <0.05.

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: NVP-HSP990 alters the life state of host cells. Caco-2 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3) and further cultivated with DMEM containing 100 nM NVP-HSP990 or an equal volume of DMSO as a control for 24 h. Then, the infected cells were harvested for RNA-seq analysis. ( A ) Multiple differential scatter plots of compared groups. ( B ) Venn diagrams of up- and downregulated genes between compared groups. ( C, D ) Top 10 (ranked by descending Q value) upregulated ( C ) and downregulated ( D ) KEGG pathways in all mock-, Wa-, and SA11-infected Caco-2 cells. ( E, F ) Top 10 (ranked by descending Q value) upregulated ( E ) and downregulated ( F ) KEGG pathways in both Wa- and SA11-infected but not in mock-infected Caco-2 cells. *Q value <0.05.

Article Snippet: Human intestinal epithelial cell lines Caco-2 cells (ATCC: HTB-37) and HT-29 cells (ATCC: HTB-38) were from ATCC and kept in our institute.

Techniques: Infection, Control, RNA Sequencing

NVP-HSP990 inhibited MAPK activation and facilitated expression of tight junction-associated proteins in intestinal cells. ( A ) MA104, Caco-2, and HT-29 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3), followed by treatment of 100 nM HSP990 (+) or an equal volume of DMSO as a control (−) for 20 h. Then the infected cells were harvested for WB analysis of MAPK components. ( B ) Caco-2 cells were mock-infected with PBS, treated with 1 µM C16-PAF(C16), or infected with RV Wa or SA11 strains (MOI = 3), and then treated with 100 nM HSP990 (+) or DMSO as a control (−) for 20 h. The infected cells were harvested for WB analysis of MAPK components. ( C ) Caco-2 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3), and then treated with 100 nM HSP990 (+) or DMSO as control (−) for 20 h. Then the infected cells were harvested for WB analysis of tight junction-associated proteins. Data are representative of three ( A ) and two ( B and C ) independent experiments.

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: NVP-HSP990 inhibited MAPK activation and facilitated expression of tight junction-associated proteins in intestinal cells. ( A ) MA104, Caco-2, and HT-29 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3), followed by treatment of 100 nM HSP990 (+) or an equal volume of DMSO as a control (−) for 20 h. Then the infected cells were harvested for WB analysis of MAPK components. ( B ) Caco-2 cells were mock-infected with PBS, treated with 1 µM C16-PAF(C16), or infected with RV Wa or SA11 strains (MOI = 3), and then treated with 100 nM HSP990 (+) or DMSO as a control (−) for 20 h. The infected cells were harvested for WB analysis of MAPK components. ( C ) Caco-2 cells were mock-infected with PBS or infected with RV Wa or SA11 strains (MOI = 3), and then treated with 100 nM HSP990 (+) or DMSO as control (−) for 20 h. Then the infected cells were harvested for WB analysis of tight junction-associated proteins. Data are representative of three ( A ) and two ( B and C ) independent experiments.

Article Snippet: Human intestinal epithelial cell lines Caco-2 cells (ATCC: HTB-37) and HT-29 cells (ATCC: HTB-38) were from ATCC and kept in our institute.

Techniques: Activation Assay, Expressing, Infection, Control

NVP-HSP990 mitigated disruption of tight junctions in RV infection. Caco-2 cells growing on coverslips were mock-infected or infected with RV Wa or SA11 strains (MOI = 3), and cultivated with DMEM containing 100 nM NVP-HSP990 or an equal volume of DMSO as a control after infection for another 18 h. Then the infected cells were applied for immunostaining for RV antigens (green), ZO-1 (red), and DAPI staining of nucleus (blue). Data are representative of two independent experiments.

Journal: Journal of Virology

Article Title: A small-molecule HSP90 inhibitor, NVP-HSP990, alleviates rotavirus infection

doi: 10.1128/jvi.01883-25

Figure Lengend Snippet: NVP-HSP990 mitigated disruption of tight junctions in RV infection. Caco-2 cells growing on coverslips were mock-infected or infected with RV Wa or SA11 strains (MOI = 3), and cultivated with DMEM containing 100 nM NVP-HSP990 or an equal volume of DMSO as a control after infection for another 18 h. Then the infected cells were applied for immunostaining for RV antigens (green), ZO-1 (red), and DAPI staining of nucleus (blue). Data are representative of two independent experiments.

Article Snippet: Human intestinal epithelial cell lines Caco-2 cells (ATCC: HTB-37) and HT-29 cells (ATCC: HTB-38) were from ATCC and kept in our institute.

Techniques: Disruption, Infection, Control, Immunostaining, Staining

Reduced SNORD93 expression in CRC. (A) Expression levels of the SNORD93 mRNA in 13 CRC tissues and paired adjacent tissues were determined via qRT-PCR analysis (P=0.03), normalized to 18S rRNA. (B) Expression levels of the SNORD93 mRNA in CRC cell lines (SW480, HT-29, and HCT-15) relative to normal HIEC controls, quantified by qRT-PCR analysis (HIEC: SW480, P<0.001; HIEC: HT-29, P<0.001; HIEC: HCT-15, P=0.002). (C) Prognostic relevance of SNORD93 abundance in colorectal cancer survival outcomes. Green color indicates patients with CRC and low SNORD93 expression, while red color indicates patients with CRC and high SNORD93 expression (P=0.001). Data are presented as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CRC, colorectal cancer; HIEC, human intestinal epithelial crypt cell; mRNA, messenger RNA; NT, normal tissue samples; qRT-PCR, quantitative real-time polymerase chain reaction; rRNA, ribosomal RNA; SD, standard deviation; T, tissue samples.

Journal: Translational Cancer Research

Article Title: SNORD93 suppresses colorectal cancer progression by inducing G0/G1 arrest and apoptosis

doi: 10.21037/tcr-2025-1236

Figure Lengend Snippet: Reduced SNORD93 expression in CRC. (A) Expression levels of the SNORD93 mRNA in 13 CRC tissues and paired adjacent tissues were determined via qRT-PCR analysis (P=0.03), normalized to 18S rRNA. (B) Expression levels of the SNORD93 mRNA in CRC cell lines (SW480, HT-29, and HCT-15) relative to normal HIEC controls, quantified by qRT-PCR analysis (HIEC: SW480, P<0.001; HIEC: HT-29, P<0.001; HIEC: HCT-15, P=0.002). (C) Prognostic relevance of SNORD93 abundance in colorectal cancer survival outcomes. Green color indicates patients with CRC and low SNORD93 expression, while red color indicates patients with CRC and high SNORD93 expression (P=0.001). Data are presented as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CRC, colorectal cancer; HIEC, human intestinal epithelial crypt cell; mRNA, messenger RNA; NT, normal tissue samples; qRT-PCR, quantitative real-time polymerase chain reaction; rRNA, ribosomal RNA; SD, standard deviation; T, tissue samples.

Article Snippet: The human CRC cell lines HT-29 (HTB-38), SW480 (CCL-228), and HCT-15 (CCL-225), and the normal human intestinal epithelial crypt cell (HIEC) line (CRL-3266) were sourced from the American Type Culture Collection (ATCC; Manassas, VI, USA).

Techniques: Expressing, Quantitative RT-PCR, Real-time Polymerase Chain Reaction, Standard Deviation

(a) Time- and dose-dependent loss of HT29 viability after treatment with p80 (0–0.25 %) for 3–10 h quantified by Sytox Green uptake, CellTiter-Blue and -Glo assays. (b) Sytox Green micrographs of HT29 cells exposed to 0.25 % p80 (6 h, 10 h). Scale bar, 400 µm. (c) Murine intestinal organoids treated with p80 (0.01–0.25 %) for 30 min–6 h: Sytox Green images (up; scale bar, 400 µm) and CellTiter-Glo viability (down). (d) GO and KEGG enrichment of differentially expressed genes in HT29 cells after 2 h 0.25% p80 treatment. (e, f) KEGG ferroptosis (e) and autophagy (f) pathways map highlighting p80-regulated genes. Nodes are colored by RNA-seq differential expression where red = upregulated transcripts (log₂FC > 0), green = downregulated transcripts (log₂FC < 0); grey = not detected/not significant (FDR < 0.05 where shown). (g) Rescue assay: viability of HT29 cells treated with p80 for 8 h and 24 h in the presence of apoptosis (VX-765, zVAD), autophagy (Rapamycin, Trehalose), necroptosis (Nec-1), ROS (NAC) or ferroptosis (Ferrostatin-1, RSL3) inhibitors. (h) Sytox Green staining of HT29 cells treated with 0.25% p80 for 8 h in the presence of Ferroptosis (Fer-1) and ROS (NAC) inhibitors and stained with Hoechst (blue) and Sytox Green (green). Scale bars: 400 μm. Data presented as mean ± SD. (n = 3). Statistical significance was assessed by one-way ANOVA with Tukey’s post-hoc test (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 versus non-treated, NT in a and vs p80 in g). Images are representative of ≥ 3 independent experiments.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) Time- and dose-dependent loss of HT29 viability after treatment with p80 (0–0.25 %) for 3–10 h quantified by Sytox Green uptake, CellTiter-Blue and -Glo assays. (b) Sytox Green micrographs of HT29 cells exposed to 0.25 % p80 (6 h, 10 h). Scale bar, 400 µm. (c) Murine intestinal organoids treated with p80 (0.01–0.25 %) for 30 min–6 h: Sytox Green images (up; scale bar, 400 µm) and CellTiter-Glo viability (down). (d) GO and KEGG enrichment of differentially expressed genes in HT29 cells after 2 h 0.25% p80 treatment. (e, f) KEGG ferroptosis (e) and autophagy (f) pathways map highlighting p80-regulated genes. Nodes are colored by RNA-seq differential expression where red = upregulated transcripts (log₂FC > 0), green = downregulated transcripts (log₂FC < 0); grey = not detected/not significant (FDR < 0.05 where shown). (g) Rescue assay: viability of HT29 cells treated with p80 for 8 h and 24 h in the presence of apoptosis (VX-765, zVAD), autophagy (Rapamycin, Trehalose), necroptosis (Nec-1), ROS (NAC) or ferroptosis (Ferrostatin-1, RSL3) inhibitors. (h) Sytox Green staining of HT29 cells treated with 0.25% p80 for 8 h in the presence of Ferroptosis (Fer-1) and ROS (NAC) inhibitors and stained with Hoechst (blue) and Sytox Green (green). Scale bars: 400 μm. Data presented as mean ± SD. (n = 3). Statistical significance was assessed by one-way ANOVA with Tukey’s post-hoc test (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 versus non-treated, NT in a and vs p80 in g). Images are representative of ≥ 3 independent experiments.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: RNA Sequencing, Quantitative Proteomics, Rescue Assay, Staining

(a) ROS by H₂DCFDA flow cytometry. Left: FITC-A (H₂DCFDA, 488) fluorescence (a.u.) density histograms (bi-exponential) for live singlets after 0, 1, 3, 6, 10, 24 h with 0.25% p80 vs NT. Right: ROS MFI (FITC), normalized to NT (=1). % ROS-positive (FMO-defined) is provided in Supplementary Fig. 6. (b) Confocal ROS images of HT29 cells after 1 h and 3 h 0.25% p80; ROS, green; nuclei, Hoechst (blue). Scale bar, 100 µm. (c) Seahorse XF Cell Mito Stress Test after 3 h p80. Bars show OCR (pmol O₂·min⁻¹) parameters: basal respiration, maximal respiration, proton leak, spare respiratory capacity, non-mitochondrial OCR, and ATP production. (d) ΔΨm by JC-1 flow cytometry. Left: FITC (530/30; JC-1 monomers, green) and PE-TxRed (610/20; JC-1 aggregates, red) histograms (bi-exponential) for live singlets. Right: JC-1 red/green ratio = median(PE-TxRed 610/20 ÷ FITC 530/30) per cell, normalized to NT (=1). Detail on Supplementary Fig. 6. (e) Transmission electron microscopy (TEM) ultrastructure of HT29 cells treated with 0.25% p80 for 3, 6 and 10 h; orange arrows mark mitochondria structural changes. Scale bar, 1 µm. (f) Lipid peroxidation by BODIPY 581/591 C11. Left: density histograms (bi-exponential) for live singlets showing oxidized (FITC 530/30) and non-oxidized (PE 585/42) C11 signals over 0–24 h after 0.25% p80 vs NT). Detail on Supplementary Fig. 6. (g) Confocal BODIPY 581/591 C11 at 1, 3, and 6 h: oxidized (green, 510 nm) and non-oxidized (red, 590 nm); nuclei Hoechst. Scale bar, 200 µm. Unless stated otherwise, graphs show mean ± SD from ≥3 independent experiments. One-way ANOVA (Tukey): *p < 0.05, **p < 0.01, ***p < 0.001, ***p < 0.0001 vs NT.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) ROS by H₂DCFDA flow cytometry. Left: FITC-A (H₂DCFDA, 488) fluorescence (a.u.) density histograms (bi-exponential) for live singlets after 0, 1, 3, 6, 10, 24 h with 0.25% p80 vs NT. Right: ROS MFI (FITC), normalized to NT (=1). % ROS-positive (FMO-defined) is provided in Supplementary Fig. 6. (b) Confocal ROS images of HT29 cells after 1 h and 3 h 0.25% p80; ROS, green; nuclei, Hoechst (blue). Scale bar, 100 µm. (c) Seahorse XF Cell Mito Stress Test after 3 h p80. Bars show OCR (pmol O₂·min⁻¹) parameters: basal respiration, maximal respiration, proton leak, spare respiratory capacity, non-mitochondrial OCR, and ATP production. (d) ΔΨm by JC-1 flow cytometry. Left: FITC (530/30; JC-1 monomers, green) and PE-TxRed (610/20; JC-1 aggregates, red) histograms (bi-exponential) for live singlets. Right: JC-1 red/green ratio = median(PE-TxRed 610/20 ÷ FITC 530/30) per cell, normalized to NT (=1). Detail on Supplementary Fig. 6. (e) Transmission electron microscopy (TEM) ultrastructure of HT29 cells treated with 0.25% p80 for 3, 6 and 10 h; orange arrows mark mitochondria structural changes. Scale bar, 1 µm. (f) Lipid peroxidation by BODIPY 581/591 C11. Left: density histograms (bi-exponential) for live singlets showing oxidized (FITC 530/30) and non-oxidized (PE 585/42) C11 signals over 0–24 h after 0.25% p80 vs NT). Detail on Supplementary Fig. 6. (g) Confocal BODIPY 581/591 C11 at 1, 3, and 6 h: oxidized (green, 510 nm) and non-oxidized (red, 590 nm); nuclei Hoechst. Scale bar, 200 µm. Unless stated otherwise, graphs show mean ± SD from ≥3 independent experiments. One-way ANOVA (Tukey): *p < 0.05, **p < 0.01, ***p < 0.001, ***p < 0.0001 vs NT.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: Flow Cytometry, Fluorescence, Transmission Assay, Electron Microscopy

(a) Mitochondrial Fe²⁺ by Mito-FerroGreen (flow cytometry). Left: AF488-A (Mito-FerroGreen) fluorescence (a.u.) density histograms (bi-exponential) for live singlets at 1–24 h after 0.25% p80 vs NT. Right: % Mito-FerroGreen-positive (of live singlets); gate set with unstained + AF488 FMO; single-stain compensation applied. Percent data were analyzed after arcsine–square-root transform. Detailed provided in Supplementary Fig. 6. (b) Cytosolic labile iron levels measured by FerroOrange staining under 0.25 % p80 for 0–24 h; histograms (left) and quantification (percentage of positive cells, right) shown. Detailed provided in Supplementary Fig. 6. (c, d) Western blot analysis of ferroptosis-related proteins (4F2hc, xCT/SLC7A11, NCOA4, FTH1, GPX4) and oxidative stress markers (Nrf2, HO-1, Keap1) in HT29 cells treated with p80 over time; β-actin, GAPDH, and Tubulin are used as loading controls. Graphs show mean ± SD from three independent biological experiments. Statistical significance determined by one-way ANOVA with Tukey’s test (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 versus non-treated, NT). Images are representative of ≥ 3 independent experiments.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) Mitochondrial Fe²⁺ by Mito-FerroGreen (flow cytometry). Left: AF488-A (Mito-FerroGreen) fluorescence (a.u.) density histograms (bi-exponential) for live singlets at 1–24 h after 0.25% p80 vs NT. Right: % Mito-FerroGreen-positive (of live singlets); gate set with unstained + AF488 FMO; single-stain compensation applied. Percent data were analyzed after arcsine–square-root transform. Detailed provided in Supplementary Fig. 6. (b) Cytosolic labile iron levels measured by FerroOrange staining under 0.25 % p80 for 0–24 h; histograms (left) and quantification (percentage of positive cells, right) shown. Detailed provided in Supplementary Fig. 6. (c, d) Western blot analysis of ferroptosis-related proteins (4F2hc, xCT/SLC7A11, NCOA4, FTH1, GPX4) and oxidative stress markers (Nrf2, HO-1, Keap1) in HT29 cells treated with p80 over time; β-actin, GAPDH, and Tubulin are used as loading controls. Graphs show mean ± SD from three independent biological experiments. Statistical significance determined by one-way ANOVA with Tukey’s test (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 versus non-treated, NT). Images are representative of ≥ 3 independent experiments.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: Flow Cytometry, Fluorescence, Staining, Western Blot

(a) Cell viability (CellTiter-Glo) at 3, 6, and 10 h after treatment with 0.25 % p80 and Ferroptosis inhibitors Liproxstatin-1 (Lip), Tocopherol (Toco), Deferoxamine (DFO), or Zileuton (Zil); DMSO as vehicle control. Y-axis = Viability (% of time-matched DMSO = 100%). (b) Transmission electron microscopy (TEM) of mitochondrial ultrastructure at 10 h after treatment with DMSO, p80, or p80 co-treated with Fer or DFO; scale bar, 1 µm. (c) Western blot analysis of ferroptosis markers (GPX4, SLC7A11, FTH1) and oxidative stress marker HO-1 at 10 h post p80 ± Fer; β-actin, GAPDH, and Tubulin used as loading/housekeeping controls. (d, e) Confocal microscopy showing lipid peroxidation (D, red fluorescence) and ROS production (E, green fluorescence) in HT29 cells at 3 h post-p80 and Fer-treatment; scale bars, 50 µm. (f) Malondialdehyde (MDA) in small-intestinal loops from live C57BL/6 female mice treated for 2 h with vehicle (DMSO in PBS), 1% polysorbate-80 (p80), or p80 + 10 µM Ferrostatin-1 (Fer). Mice per group: DMSO n=4; p80 n=5; p80+Fer n=5. Graphs show mean ± SD from three independent biological experiments. Statistical significance determined by one-way ANOVA with Tukey’s test (*P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 versus control). (f) ****P < 0.0001 versus DMSO control and $$$$ P < 0.0001 versus p80.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) Cell viability (CellTiter-Glo) at 3, 6, and 10 h after treatment with 0.25 % p80 and Ferroptosis inhibitors Liproxstatin-1 (Lip), Tocopherol (Toco), Deferoxamine (DFO), or Zileuton (Zil); DMSO as vehicle control. Y-axis = Viability (% of time-matched DMSO = 100%). (b) Transmission electron microscopy (TEM) of mitochondrial ultrastructure at 10 h after treatment with DMSO, p80, or p80 co-treated with Fer or DFO; scale bar, 1 µm. (c) Western blot analysis of ferroptosis markers (GPX4, SLC7A11, FTH1) and oxidative stress marker HO-1 at 10 h post p80 ± Fer; β-actin, GAPDH, and Tubulin used as loading/housekeeping controls. (d, e) Confocal microscopy showing lipid peroxidation (D, red fluorescence) and ROS production (E, green fluorescence) in HT29 cells at 3 h post-p80 and Fer-treatment; scale bars, 50 µm. (f) Malondialdehyde (MDA) in small-intestinal loops from live C57BL/6 female mice treated for 2 h with vehicle (DMSO in PBS), 1% polysorbate-80 (p80), or p80 + 10 µM Ferrostatin-1 (Fer). Mice per group: DMSO n=4; p80 n=5; p80+Fer n=5. Graphs show mean ± SD from three independent biological experiments. Statistical significance determined by one-way ANOVA with Tukey’s test (*P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 versus control). (f) ****P < 0.0001 versus DMSO control and $$$$ P < 0.0001 versus p80.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: Control, Transmission Assay, Electron Microscopy, Western Blot, Marker, Confocal Microscopy, Fluorescence

(a) RNA-seq network of differentially expressed genes in HT29 cells treated with 0.25% p80, highlighting upregulated (red) and downregulated (blue) genes in lipid metabolism and ferroptosis pathways. (b) Gene Ontology (GO) enrichment of lipid metabolism–related pathways activated by 0.25% p80. (c) Transmission electron microscopy (TEM) of HT29 cells over 10 h of 0.25% p80 treatment; orange arrows mark lipid droplets. Scale bar: 1 µm. (d) Confocal images and quantification of BODIPY-stained lipid droplets in HT29 cells treated with 0.25% p80 for 6 h and 24 h; scale bar: 400 µm. Left, relative per centage BODIPY-stained area, data are mean ± SEM (n = 3); one-way ANOVA with Tukey’s post hoc (**p < 0.01; ***p < 0.001 versus NT). (e) Neutral lipid droplets by BODIPY 493/503 flow cytometry after 0.25% p80 for 3 h (left) and 10 h (right) ± inhibitors (Avasimibe, PF-04620110 [DGAT1], A-922500 [DGAT1], PF-06424439 [DGAT2], Atglistatin [ATGL], TOFA [ACC], A939572 [SCD1], TVB-3166 [FASN], Carbenoxolone, T863 [DGAT1]) or Ferrostatin-1 (Fer).Y-axis: % BODIPY-high cells (AF488-A, 530/30; live singlets). For more detail go to Supplementary figure 6. (f) CellTiter-Glo viability at 6 h and 10 h in HT29 cells treated with 0.25% p80 ± PF-04620110, (DGAT1), TOFA (ACC), or Ferrostatin-1 (Fer), alone or combined. X-axis: treatment groups (NT, p80, p80+PF, p80+TOFA, p80+Fer, combos). Y-axis: Viability (% of time-matched NT = 100%). Mean ± SEM (n = 3); one-way ANOVA with Tukey’s (*p < 0.05; **p < 0.01; ***p < 0.001). (g) Confocal BODIPY images of HT29 cells transfected with PLIN2 siRNA versus non-targeting control after 0.25% p80 treatment; scale bar: 400 µm. Representative of three experiments.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) RNA-seq network of differentially expressed genes in HT29 cells treated with 0.25% p80, highlighting upregulated (red) and downregulated (blue) genes in lipid metabolism and ferroptosis pathways. (b) Gene Ontology (GO) enrichment of lipid metabolism–related pathways activated by 0.25% p80. (c) Transmission electron microscopy (TEM) of HT29 cells over 10 h of 0.25% p80 treatment; orange arrows mark lipid droplets. Scale bar: 1 µm. (d) Confocal images and quantification of BODIPY-stained lipid droplets in HT29 cells treated with 0.25% p80 for 6 h and 24 h; scale bar: 400 µm. Left, relative per centage BODIPY-stained area, data are mean ± SEM (n = 3); one-way ANOVA with Tukey’s post hoc (**p < 0.01; ***p < 0.001 versus NT). (e) Neutral lipid droplets by BODIPY 493/503 flow cytometry after 0.25% p80 for 3 h (left) and 10 h (right) ± inhibitors (Avasimibe, PF-04620110 [DGAT1], A-922500 [DGAT1], PF-06424439 [DGAT2], Atglistatin [ATGL], TOFA [ACC], A939572 [SCD1], TVB-3166 [FASN], Carbenoxolone, T863 [DGAT1]) or Ferrostatin-1 (Fer).Y-axis: % BODIPY-high cells (AF488-A, 530/30; live singlets). For more detail go to Supplementary figure 6. (f) CellTiter-Glo viability at 6 h and 10 h in HT29 cells treated with 0.25% p80 ± PF-04620110, (DGAT1), TOFA (ACC), or Ferrostatin-1 (Fer), alone or combined. X-axis: treatment groups (NT, p80, p80+PF, p80+TOFA, p80+Fer, combos). Y-axis: Viability (% of time-matched NT = 100%). Mean ± SEM (n = 3); one-way ANOVA with Tukey’s (*p < 0.05; **p < 0.01; ***p < 0.001). (g) Confocal BODIPY images of HT29 cells transfected with PLIN2 siRNA versus non-targeting control after 0.25% p80 treatment; scale bar: 400 µm. Representative of three experiments.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: RNA Sequencing, Transmission Assay, Electron Microscopy, Staining, Flow Cytometry, Transfection, Control

(a) Heatmap of differentially expressed triglycerides in HT29 cells at 10 hours post-treatment with 0.25% p80 compared to non-treated (NT) controls. (b) Heatmap showing the effects of Ferrostatin-1 (Fer), TOFA, and a DGAT inhibitor on 0.25% p80-induced triglyceride accumulation at 10 hours post-treatment. (c) Heatmap of polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) at 2, 6, and 10 hours post-treatment with 0.25% p80. (d, e) Heatmaps of PUFAs and MUFAs highlighting the impact of lipid metabolism inhibitors at 3 hours (d) and 10 hours (e) on 0.25% p80-induced lipid alterations. NT = non-treated control. Values are log2 fold-changes vs time-matched NT from aligned, median-normalized LC–MS intensities. A 16:0 sphingomyelin internal standard monitored extraction and instrument stability. Red = increase; blue = decrease.

Journal: bioRxiv

Article Title: The dietary emulsifier polysorbate-80 induces lipid accumulation and cell death in intestinal epithelial cells via ferroptosis

doi: 10.1101/2025.08.29.673091

Figure Lengend Snippet: (a) Heatmap of differentially expressed triglycerides in HT29 cells at 10 hours post-treatment with 0.25% p80 compared to non-treated (NT) controls. (b) Heatmap showing the effects of Ferrostatin-1 (Fer), TOFA, and a DGAT inhibitor on 0.25% p80-induced triglyceride accumulation at 10 hours post-treatment. (c) Heatmap of polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) at 2, 6, and 10 hours post-treatment with 0.25% p80. (d, e) Heatmaps of PUFAs and MUFAs highlighting the impact of lipid metabolism inhibitors at 3 hours (d) and 10 hours (e) on 0.25% p80-induced lipid alterations. NT = non-treated control. Values are log2 fold-changes vs time-matched NT from aligned, median-normalized LC–MS intensities. A 16:0 sphingomyelin internal standard monitored extraction and instrument stability. Red = increase; blue = decrease.

Article Snippet: Human intestinal epithelial cell lines HT29 (ATCC HTB-38), C2BBe1 (ATCC CRL-2102) and DLD-1 (ATCC CCL-221), were obtained from the American Type Culture Collection (ATCC).

Techniques: Control, Liquid Chromatography with Mass Spectroscopy, Extraction

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