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Servicebio Inc endometrial cancer cell lines hec 1 a
S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 <t>probe</t> <t>after</t> <t>HEC-1-A</t> and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
Endometrial Cancer Cell Lines Hec 1 A, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
endometrial cancer cell lines hec 1 a - by Bioz Stars, 2026-07
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Images

1) Product Images from "Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer"

Article Title: Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer

Journal: Biomedicines

doi: 10.3390/biomedicines14030608

S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 probe after HEC-1-A and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
Figure Legend Snippet: S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 probe after HEC-1-A and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Techniques Used: CCK-8 Assay, Positive Control, Flow Cytometry, Fluorescence, Control

ACSL4 mediates S.C-induced ferroptosis in endometrial cancer cells. ( A , B ) Representative WB showing ACSL4 protein levels in the indicated cell lines. ( C , D ) The viability of indicated cells following a 48 h treatment with 1.0 μM S.C was determined by the CCK-8 assay. ( E , F ) WB analysis of FTH and ACSL4 protein levels in HEC-1-A and AN3CA cells co-treated with 1.0 μM S.C and 30 μM Berberine for 48 h. ( G , H ) Lipid peroxidation was assessed in HEC-1-A and AN3CA cells following a 48 h concomitant treatment with 1.0 μM S.C and 30 μM Berberine, using the C11-BODIPY 581/591 probe. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
Figure Legend Snippet: ACSL4 mediates S.C-induced ferroptosis in endometrial cancer cells. ( A , B ) Representative WB showing ACSL4 protein levels in the indicated cell lines. ( C , D ) The viability of indicated cells following a 48 h treatment with 1.0 μM S.C was determined by the CCK-8 assay. ( E , F ) WB analysis of FTH and ACSL4 protein levels in HEC-1-A and AN3CA cells co-treated with 1.0 μM S.C and 30 μM Berberine for 48 h. ( G , H ) Lipid peroxidation was assessed in HEC-1-A and AN3CA cells following a 48 h concomitant treatment with 1.0 μM S.C and 30 μM Berberine, using the C11-BODIPY 581/591 probe. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Techniques Used: CCK-8 Assay, Control

S.C suppresses FTO to upregulate ACSL4 and to promote lipid peroxidation. ( A , B ) WB analysis of protein levels of ALKBH5, METTL3, USP15, FTO, SENP1, and TRIM21 in HEC-1-A and AN3CA cells treated with 0, 0.5, or 1.0 μM S.C for 48 h. ( C ) Analysis of ACSL4 and FTO protein expression by WB in FTO-overexpressing cells with or without 1.0 μM S.C treatment. ( D , E ) Lipid peroxidation was evaluated in FTO-overexpressing cells following treatment with 1.0 μM S.C or under control conditions, using the C11-BODIPY 581/591 probe.
Figure Legend Snippet: S.C suppresses FTO to upregulate ACSL4 and to promote lipid peroxidation. ( A , B ) WB analysis of protein levels of ALKBH5, METTL3, USP15, FTO, SENP1, and TRIM21 in HEC-1-A and AN3CA cells treated with 0, 0.5, or 1.0 μM S.C for 48 h. ( C ) Analysis of ACSL4 and FTO protein expression by WB in FTO-overexpressing cells with or without 1.0 μM S.C treatment. ( D , E ) Lipid peroxidation was evaluated in FTO-overexpressing cells following treatment with 1.0 μM S.C or under control conditions, using the C11-BODIPY 581/591 probe.

Techniques Used: Expressing, Control

S.C inhibits endometrial tumor growth by triggering ferroptosis in vivo. ( A ) Mice bearing HEC-1-A xenografts were treated intraperitoneally with S.C or PBS once every two days ( n = 6 in each group) for a total of 14 days. ( B ) Tumors were harvested and photographed. ( C ) Tumor weights were measured and compared across groups. ( D , E ) Representative images of H&E staining and IHC staining for Ki67 are presented. ( F ) Protein expression levels of ACSL4, FTH, FTL, NCOA4, NRF2, and GPX4 were assessed by WB analysis. Data are presented as means ± SD. * p < 0.05; n.s, not significant.
Figure Legend Snippet: S.C inhibits endometrial tumor growth by triggering ferroptosis in vivo. ( A ) Mice bearing HEC-1-A xenografts were treated intraperitoneally with S.C or PBS once every two days ( n = 6 in each group) for a total of 14 days. ( B ) Tumors were harvested and photographed. ( C ) Tumor weights were measured and compared across groups. ( D , E ) Representative images of H&E staining and IHC staining for Ki67 are presented. ( F ) Protein expression levels of ACSL4, FTH, FTL, NCOA4, NRF2, and GPX4 were assessed by WB analysis. Data are presented as means ± SD. * p < 0.05; n.s, not significant.

Techniques Used: In Vivo, Staining, Immunohistochemistry, Expressing



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S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 <t>probe</t> <t>after</t> <t>HEC-1-A</t> and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
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S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 <t>probe</t> <t>after</t> <t>HEC-1-A</t> and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
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S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 <t>probe</t> <t>after</t> <t>HEC-1-A</t> and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.
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Image Search Results


(A, B) Kaplan-Meier plots showing that LARP1 overexpression is associated with shorter overall survival (A) and progression-free interval (B) in endometrial cancer cohort (n=454). (C) Immunoblot analysis illustrating the protein expression of LARP1 after transfecting ISHI cell line with control or LARP1 siRNA at 25, 50, 75, and 100 nM. β-actin was used as a loading control. (D) Images derived from immunofluorescence analysis showing the protein expression of LARP1 after transfecting HEC-1A cells with control or LARP1 siRNA at 75 µM. Scale bar = 50 µM.

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Kaplan-Meier plots showing that LARP1 overexpression is associated with shorter overall survival (A) and progression-free interval (B) in endometrial cancer cohort (n=454). (C) Immunoblot analysis illustrating the protein expression of LARP1 after transfecting ISHI cell line with control or LARP1 siRNA at 25, 50, 75, and 100 nM. β-actin was used as a loading control. (D) Images derived from immunofluorescence analysis showing the protein expression of LARP1 after transfecting HEC-1A cells with control or LARP1 siRNA at 75 µM. Scale bar = 50 µM.

Article Snippet: Human endometrial cancer cell lines HEC-1A and Ishikawa (ISHI) were obtained from ATCC (American Type Culture Collection, Manassas, VA, USA).

Techniques: Over Expression, Western Blot, Expressing, Control, Derivative Assay, Immunofluorescence

(A – D) Cell viability assay showing the effect of two different LARP1 siRNA (1 and 2) on the viability of ISHI (A, B) and HEC-1A (C, D) cell lines. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots. (E) Immunoblot analysis showing the protein expression of cleaved PARP1 and cleaved caspase 3 after transfection of ISHI and HEC-1A cells with control or LARP1 siRNAs. β-actin was used as a loading control.

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A – D) Cell viability assay showing the effect of two different LARP1 siRNA (1 and 2) on the viability of ISHI (A, B) and HEC-1A (C, D) cell lines. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots. (E) Immunoblot analysis showing the protein expression of cleaved PARP1 and cleaved caspase 3 after transfection of ISHI and HEC-1A cells with control or LARP1 siRNAs. β-actin was used as a loading control.

Article Snippet: Human endometrial cancer cell lines HEC-1A and Ishikawa (ISHI) were obtained from ATCC (American Type Culture Collection, Manassas, VA, USA).

Techniques: Viability Assay, Western Blot, Expressing, Transfection, Control

(A, B) Immunoblot analysis showing the protein expression of LARP1 and E2F1 after transfecting ISHI (A) and HEC-1A (B) cells with control or LARP1 siRNA. β-actin was used as a loading control. (C) Images representing immunofluorescence staining of LARP1 (green) and E2F1 (red) in HEC-1A cells after transfection with control or LARP1 siRNA. DAPI was used as a counter stain. Scale bar = 50 µm.

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) Immunoblot analysis showing the protein expression of LARP1 and E2F1 after transfecting ISHI (A) and HEC-1A (B) cells with control or LARP1 siRNA. β-actin was used as a loading control. (C) Images representing immunofluorescence staining of LARP1 (green) and E2F1 (red) in HEC-1A cells after transfection with control or LARP1 siRNA. DAPI was used as a counter stain. Scale bar = 50 µm.

Article Snippet: Human endometrial cancer cell lines HEC-1A and Ishikawa (ISHI) were obtained from ATCC (American Type Culture Collection, Manassas, VA, USA).

Techniques: Western Blot, Expressing, Control, Immunofluorescence, Staining, Transfection

(A, B) MTS cell viability assay showing the effect of escalating concentration of carboplatin on the viability of ISHI (A) and HEC-1A cell lines. Sterile water was used as a vehicle control. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots.

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, B) MTS cell viability assay showing the effect of escalating concentration of carboplatin on the viability of ISHI (A) and HEC-1A cell lines. Sterile water was used as a vehicle control. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots.

Article Snippet: Human endometrial cancer cell lines HEC-1A and Ishikawa (ISHI) were obtained from ATCC (American Type Culture Collection, Manassas, VA, USA).

Techniques: Viability Assay, Concentration Assay, Sterility, Control

(A, C) Micrographs representing colony formation assay showing the effect of LARP1 transfection and carboplatin treatment on the clonogenic survival of ISHI (A) and HEC-1A (B) cell lines. (B, D) Quantitative analysis of clonogenic assay showing the effect of LARP1 knockdown and carboplatin treatment on the clonogenic survival of ISHI (B) and HEC-1A (D) cells. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots.

Journal: bioRxiv

Article Title: “Targeting LARP1 Enhances Carboplatin Sensitivity and Suppresses Tumor Growth in Endometrial Cancer”

doi: 10.64898/2026.03.22.713473

Figure Lengend Snippet: (A, C) Micrographs representing colony formation assay showing the effect of LARP1 transfection and carboplatin treatment on the clonogenic survival of ISHI (A) and HEC-1A (B) cell lines. (B, D) Quantitative analysis of clonogenic assay showing the effect of LARP1 knockdown and carboplatin treatment on the clonogenic survival of ISHI (B) and HEC-1A (D) cells. One-way analysis of variance (ANOVA) was used to assess statistical significance among groups, followed by Tukey’s post hoc test for multiple pairwise comparisons. Data are presented as mean ± SD, with individual data points shown as dots.

Article Snippet: Human endometrial cancer cell lines HEC-1A and Ishikawa (ISHI) were obtained from ATCC (American Type Culture Collection, Manassas, VA, USA).

Techniques: Colony Assay, Transfection, Clonogenic Assay, Knockdown

S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 probe after HEC-1-A and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Journal: Biomedicines

Article Title: Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer

doi: 10.3390/biomedicines14030608

Figure Lengend Snippet: S.C provokes ferroptosis in EC cells. ( A , B ) EC cells were treated with S.C (1.0 μM) for 48 h in the presence or absence of Fer-1 (2.0 μM) or DFO (5.0 μM), and cell viability was assessed by CCK-8 assay. ( C ) Intracellular MDA levels were quantified in EC cells treated with S.C or RSL3 (positive control) for 48 h using commercial assay kits. ( D , E ) WB analysis of protein levels of NCOA4, NRF2, ACSL4, KEAP1, SLC7A11, SLC11A2, SLC40A1, SCD, FTH, FTL, FSP1, and GPX4 in EC cells treated with S.C for 48 h. ( F , G ) Intracellular ROS levels were measured by flow cytometry using the fluorescent probe DCFH-DA (10 μM) in EC cells treated with S.C (1.0 μM) or without DFO (5.0 μM) for 48 h. ( H , I ) Lipid peroxidation was detected using C11-BODIPY 581/591 probe after HEC-1-A and AN3CA cells were treated with S.C for 48 h. Red fluorescence represents the reduction state of cells; green fluorescence represents the oxidation state of cells. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Article Snippet: The endometrial cancer cell lines HEC-1-A, AN3CA and KLE were obtained from Servicebio (Wuhan, China).

Techniques: CCK-8 Assay, Positive Control, Flow Cytometry, Fluorescence, Control

ACSL4 mediates S.C-induced ferroptosis in endometrial cancer cells. ( A , B ) Representative WB showing ACSL4 protein levels in the indicated cell lines. ( C , D ) The viability of indicated cells following a 48 h treatment with 1.0 μM S.C was determined by the CCK-8 assay. ( E , F ) WB analysis of FTH and ACSL4 protein levels in HEC-1-A and AN3CA cells co-treated with 1.0 μM S.C and 30 μM Berberine for 48 h. ( G , H ) Lipid peroxidation was assessed in HEC-1-A and AN3CA cells following a 48 h concomitant treatment with 1.0 μM S.C and 30 μM Berberine, using the C11-BODIPY 581/591 probe. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Journal: Biomedicines

Article Title: Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer

doi: 10.3390/biomedicines14030608

Figure Lengend Snippet: ACSL4 mediates S.C-induced ferroptosis in endometrial cancer cells. ( A , B ) Representative WB showing ACSL4 protein levels in the indicated cell lines. ( C , D ) The viability of indicated cells following a 48 h treatment with 1.0 μM S.C was determined by the CCK-8 assay. ( E , F ) WB analysis of FTH and ACSL4 protein levels in HEC-1-A and AN3CA cells co-treated with 1.0 μM S.C and 30 μM Berberine for 48 h. ( G , H ) Lipid peroxidation was assessed in HEC-1-A and AN3CA cells following a 48 h concomitant treatment with 1.0 μM S.C and 30 μM Berberine, using the C11-BODIPY 581/591 probe. Data are presented as means ± SD from three independent experiments. ** p < 0.01, *** p < 0.001 versus the corresponding control group.

Article Snippet: The endometrial cancer cell lines HEC-1-A, AN3CA and KLE were obtained from Servicebio (Wuhan, China).

Techniques: CCK-8 Assay, Control

S.C suppresses FTO to upregulate ACSL4 and to promote lipid peroxidation. ( A , B ) WB analysis of protein levels of ALKBH5, METTL3, USP15, FTO, SENP1, and TRIM21 in HEC-1-A and AN3CA cells treated with 0, 0.5, or 1.0 μM S.C for 48 h. ( C ) Analysis of ACSL4 and FTO protein expression by WB in FTO-overexpressing cells with or without 1.0 μM S.C treatment. ( D , E ) Lipid peroxidation was evaluated in FTO-overexpressing cells following treatment with 1.0 μM S.C or under control conditions, using the C11-BODIPY 581/591 probe.

Journal: Biomedicines

Article Title: Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer

doi: 10.3390/biomedicines14030608

Figure Lengend Snippet: S.C suppresses FTO to upregulate ACSL4 and to promote lipid peroxidation. ( A , B ) WB analysis of protein levels of ALKBH5, METTL3, USP15, FTO, SENP1, and TRIM21 in HEC-1-A and AN3CA cells treated with 0, 0.5, or 1.0 μM S.C for 48 h. ( C ) Analysis of ACSL4 and FTO protein expression by WB in FTO-overexpressing cells with or without 1.0 μM S.C treatment. ( D , E ) Lipid peroxidation was evaluated in FTO-overexpressing cells following treatment with 1.0 μM S.C or under control conditions, using the C11-BODIPY 581/591 probe.

Article Snippet: The endometrial cancer cell lines HEC-1-A, AN3CA and KLE were obtained from Servicebio (Wuhan, China).

Techniques: Expressing, Control

S.C inhibits endometrial tumor growth by triggering ferroptosis in vivo. ( A ) Mice bearing HEC-1-A xenografts were treated intraperitoneally with S.C or PBS once every two days ( n = 6 in each group) for a total of 14 days. ( B ) Tumors were harvested and photographed. ( C ) Tumor weights were measured and compared across groups. ( D , E ) Representative images of H&E staining and IHC staining for Ki67 are presented. ( F ) Protein expression levels of ACSL4, FTH, FTL, NCOA4, NRF2, and GPX4 were assessed by WB analysis. Data are presented as means ± SD. * p < 0.05; n.s, not significant.

Journal: Biomedicines

Article Title: Targeting the FTO-ACSL4 Pathway: A Novel Mechanism for Sanguinarine Chloride-Induced Ferroptosis in Endometrial Cancer

doi: 10.3390/biomedicines14030608

Figure Lengend Snippet: S.C inhibits endometrial tumor growth by triggering ferroptosis in vivo. ( A ) Mice bearing HEC-1-A xenografts were treated intraperitoneally with S.C or PBS once every two days ( n = 6 in each group) for a total of 14 days. ( B ) Tumors were harvested and photographed. ( C ) Tumor weights were measured and compared across groups. ( D , E ) Representative images of H&E staining and IHC staining for Ki67 are presented. ( F ) Protein expression levels of ACSL4, FTH, FTL, NCOA4, NRF2, and GPX4 were assessed by WB analysis. Data are presented as means ± SD. * p < 0.05; n.s, not significant.

Article Snippet: The endometrial cancer cell lines HEC-1-A, AN3CA and KLE were obtained from Servicebio (Wuhan, China).

Techniques: In Vivo, Staining, Immunohistochemistry, Expressing

Venn diagram and Volcano diagram of DEGs in the Endometriosis and Endometrial Cancer Microarray data set. DEGs in the volcano plot shown in GSE7305 (A) , GSE2339 (B) , GSE25628 (C) , and GSE17025 (D) refer to genes with P values < 0.05 and [logFC] > 1.5. Red dots indicate genes upregulated in the experimental group relative to the control group, and blue dots indicate genes downregulated in the experimental group relative to the control group. (E) , Venn diagram of intersection of DEGs from three endometrial transposition datasets. (F) , Venn diagram of differential genes in endometriosis and endometrial cancer.

Journal: Frontiers in Oncology

Article Title: Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis

doi: 10.3389/fonc.2024.1387860

Figure Lengend Snippet: Venn diagram and Volcano diagram of DEGs in the Endometriosis and Endometrial Cancer Microarray data set. DEGs in the volcano plot shown in GSE7305 (A) , GSE2339 (B) , GSE25628 (C) , and GSE17025 (D) refer to genes with P values < 0.05 and [logFC] > 1.5. Red dots indicate genes upregulated in the experimental group relative to the control group, and blue dots indicate genes downregulated in the experimental group relative to the control group. (E) , Venn diagram of intersection of DEGs from three endometrial transposition datasets. (F) , Venn diagram of differential genes in endometriosis and endometrial cancer.

Article Snippet: The human endometrial cancer cell line (HEC - 1B and Ishikawa) and the normal endometrial epithelial cell line (HEEC) were both purchased from ATCC.

Techniques: Microarray, Control

Gene Alterations and Protein Expression of hub Genes in TCGA. (A) The endometrial cancer database of GEPIA showed significant expression of 4 DEGs, compared with normal endometrial tissues, respectively. (B) Validation of hub genes by Human Protein Atlas database (C) Significant OS and DFS analysis of APOE and BGN between high and low expression on GEPIA.

Journal: Frontiers in Oncology

Article Title: Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis

doi: 10.3389/fonc.2024.1387860

Figure Lengend Snippet: Gene Alterations and Protein Expression of hub Genes in TCGA. (A) The endometrial cancer database of GEPIA showed significant expression of 4 DEGs, compared with normal endometrial tissues, respectively. (B) Validation of hub genes by Human Protein Atlas database (C) Significant OS and DFS analysis of APOE and BGN between high and low expression on GEPIA.

Article Snippet: The human endometrial cancer cell line (HEC - 1B and Ishikawa) and the normal endometrial epithelial cell line (HEEC) were both purchased from ATCC.

Techniques: Expressing, Biomarker Discovery

Correlation between hub gene expression and immune cell infiltration level in 4 endometrial carcinomas. APOE (A) , BGN (B) , BST2 (C) , and C1QB (D) expression correlated with tumor purity and infiltration levels of B cells, CD8+T cells, CD4+T cells, macrophages, neutrophils, and dendritic cells in endometrial cancer.

Journal: Frontiers in Oncology

Article Title: Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis

doi: 10.3389/fonc.2024.1387860

Figure Lengend Snippet: Correlation between hub gene expression and immune cell infiltration level in 4 endometrial carcinomas. APOE (A) , BGN (B) , BST2 (C) , and C1QB (D) expression correlated with tumor purity and infiltration levels of B cells, CD8+T cells, CD4+T cells, macrophages, neutrophils, and dendritic cells in endometrial cancer.

Article Snippet: The human endometrial cancer cell line (HEC - 1B and Ishikawa) and the normal endometrial epithelial cell line (HEEC) were both purchased from ATCC.

Techniques: Gene Expression, Expressing