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human ec cell lines  (ATCC)


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    Structured Review

    ATCC human ec cell lines
    Human Ec Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 837 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hec+1+a+cells/pm42082487-171-4-14?v=ATCC
    Average 96 stars, based on 837 article reviews
    human ec cell lines - by Bioz Stars, 2026-08
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    (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 <t>transfecting</t> <t>HEC-1A</t> cells with control or LARP1 siRNA at 75 µM. Scale bar = 50 µM.
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    (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 <t>transfecting</t> <t>HEC-1A</t> cells with control or LARP1 siRNA at 75 µM. Scale bar = 50 µM.
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    (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 <t>transfecting</t> <t>HEC-1A</t> cells with control or LARP1 siRNA at 75 µM. Scale bar = 50 µM.
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    GATA6 is a target gene of miR-196b. A : The nucleotide sequence of the miR-196b target site in GATA6 3′-UTR. Mut: contains a four-base mutation at the miR-196b target region. B : Double-luciferase reporter assays were used to detect the binding of miR-196b to the 3’-UTR region of GATA6. C - F : qPCR and WB were used to test the mRNA ( C , D ) and protein ( E , F ) levels of GATA6 in Ishikawa ( C , E ) and HEC-1 A ( D , F ) cells. (* P < 0.05, ** P < 0.01)
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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.
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    ATCC ec cell lines
    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

    GATA6 is a target gene of miR-196b. A : The nucleotide sequence of the miR-196b target site in GATA6 3′-UTR. Mut: contains a four-base mutation at the miR-196b target region. B : Double-luciferase reporter assays were used to detect the binding of miR-196b to the 3’-UTR region of GATA6. C - F : qPCR and WB were used to test the mRNA ( C , D ) and protein ( E , F ) levels of GATA6 in Ishikawa ( C , E ) and HEC-1 A ( D , F ) cells. (* P < 0.05, ** P < 0.01)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: GATA6 is a target gene of miR-196b. A : The nucleotide sequence of the miR-196b target site in GATA6 3′-UTR. Mut: contains a four-base mutation at the miR-196b target region. B : Double-luciferase reporter assays were used to detect the binding of miR-196b to the 3’-UTR region of GATA6. C - F : qPCR and WB were used to test the mRNA ( C , D ) and protein ( E , F ) levels of GATA6 in Ishikawa ( C , E ) and HEC-1 A ( D , F ) cells. (* P < 0.05, ** P < 0.01)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: Sequencing, Mutagenesis, Luciferase, Binding Assay

    miR-196b reduces EC proliferation, migration, and invasion. A - B : qPCR detection of the expression of miR-196b in Ishikawa ( A ) and HEC-1 A ( B ) cells transfected with miR-196b mimics ( a ) or anti-miR-196b ( b ). C - D : CCK-8 assays were carried out to evaluate the proliferation capacity of Ishikawa ( C ) and HEC-1 A ( D ) cells transfected with miR-196b mimics ( a ) or anti-miR-196b ( b ). E-F: Colony formation assays were utilized to assess cell growth in Ishikawa ( E ) and HEC-1 A ( F ) cells. G - H : Wound healing assays were used to measure the migration ability in Ishikawa ( G ) and HEC-1 A ( H ) cells. I - J : Transwell assays were conducted to determine the invasion ability in Ishikawa ( I ) and HEC-1 A ( J ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: miR-196b reduces EC proliferation, migration, and invasion. A - B : qPCR detection of the expression of miR-196b in Ishikawa ( A ) and HEC-1 A ( B ) cells transfected with miR-196b mimics ( a ) or anti-miR-196b ( b ). C - D : CCK-8 assays were carried out to evaluate the proliferation capacity of Ishikawa ( C ) and HEC-1 A ( D ) cells transfected with miR-196b mimics ( a ) or anti-miR-196b ( b ). E-F: Colony formation assays were utilized to assess cell growth in Ishikawa ( E ) and HEC-1 A ( F ) cells. G - H : Wound healing assays were used to measure the migration ability in Ishikawa ( G ) and HEC-1 A ( H ) cells. I - J : Transwell assays were conducted to determine the invasion ability in Ishikawa ( I ) and HEC-1 A ( J ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: Migration, Expressing, Transfection, CCK-8 Assay

    Impact of miR-196b on the cell cycle. A and C : Flow cytometry was used to detect the cell cycle distribution in Ishikawa ( A ) and HEC-1 A ( C ) cells following miR-196b mimics ( a ) and anti-miR-196b ( b ) transfection. B and D : WB to detect cyclin-associated protein levels in Ishikawa ( B ) and HEC-1 A ( D ) cells following miR-196b mimics ( a ) and anti-miR-196b ( b ) transfection. (* P < 0.05, ** P < 0.01)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: Impact of miR-196b on the cell cycle. A and C : Flow cytometry was used to detect the cell cycle distribution in Ishikawa ( A ) and HEC-1 A ( C ) cells following miR-196b mimics ( a ) and anti-miR-196b ( b ) transfection. B and D : WB to detect cyclin-associated protein levels in Ishikawa ( B ) and HEC-1 A ( D ) cells following miR-196b mimics ( a ) and anti-miR-196b ( b ) transfection. (* P < 0.05, ** P < 0.01)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: Flow Cytometry, Transfection

    miR-196b inhibits EC proliferation in vivo. A : Weight growth curve of nude mice injected with agomir-196b-treated HEC-1 A cells. B : Tumor xenografts ( a ), tumor growth curve ( b ), and tumor weight ( c ) of nude mice at the study’s conclusion. qPCR ( d ) and WB ( e ) were performed to test the expression of miR-196b ( d ) and GATA6 ( e ) in tumors. The H&E staining reveals the pathological characteristics of the tumors from nude mice ( f ). C : Expression of GATA6, VEGF, p-AKT, and p-ERK in tumors was tested by immunohistochemical. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01, *** P < 0.001)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: miR-196b inhibits EC proliferation in vivo. A : Weight growth curve of nude mice injected with agomir-196b-treated HEC-1 A cells. B : Tumor xenografts ( a ), tumor growth curve ( b ), and tumor weight ( c ) of nude mice at the study’s conclusion. qPCR ( d ) and WB ( e ) were performed to test the expression of miR-196b ( d ) and GATA6 ( e ) in tumors. The H&E staining reveals the pathological characteristics of the tumors from nude mice ( f ). C : Expression of GATA6, VEGF, p-AKT, and p-ERK in tumors was tested by immunohistochemical. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01, *** P < 0.001)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: In Vivo, Injection, Expressing, Staining, Immunohistochemical staining

    The miR-196b/GATA6 axis regulates EC proliferation, migration, and invasion. A - F : CCK8 ( A , B ), clone formation ( C , D ), and EdU assays ( E , F ) were used to detect the proliferation capacity of Ishikawa ( A , C , E ) and HEC-1 A ( B , D , F ) cells transfected with anti-miR-196b, siGATA6, and anti-miR-196b+siGATA6. G - J : Wound healing ( G , H ) and Transwell ( I , J ) assays assessing cell migration and invasion in Ishikawa ( G , I ) and HEC-1 A ( H , J ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: The miR-196b/GATA6 axis regulates EC proliferation, migration, and invasion. A - F : CCK8 ( A , B ), clone formation ( C , D ), and EdU assays ( E , F ) were used to detect the proliferation capacity of Ishikawa ( A , C , E ) and HEC-1 A ( B , D , F ) cells transfected with anti-miR-196b, siGATA6, and anti-miR-196b+siGATA6. G - J : Wound healing ( G , H ) and Transwell ( I , J ) assays assessing cell migration and invasion in Ishikawa ( G , I ) and HEC-1 A ( H , J ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: Migration, Transfection

    miR-196b regulates the EMT process and AKT/ERK signaling pathways via GATA6 in EC cells. A - B : IF staining of E-cadherin ( A ) and vimentin ( B ) in Ishikawa ( a ) and HEC-1 A ( b ) cells. C - D : WB analysis of EMT-related markers ( C ) and AKT and ERK pathway-related proteins ( D ) in Ishikawa ( a ) and HEC-1 A ( b ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01, *** P < 0.001)

    Journal: Biology Direct

    Article Title: miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer

    doi: 10.1186/s13062-026-00749-9

    Figure Lengend Snippet: miR-196b regulates the EMT process and AKT/ERK signaling pathways via GATA6 in EC cells. A - B : IF staining of E-cadherin ( A ) and vimentin ( B ) in Ishikawa ( a ) and HEC-1 A ( b ) cells. C - D : WB analysis of EMT-related markers ( C ) and AKT and ERK pathway-related proteins ( D ) in Ishikawa ( a ) and HEC-1 A ( b ) cells. (Scale bar: 100 μm, * P < 0.05, ** P < 0.01, *** P < 0.001)

    Article Snippet: Ishikawa and HEC-1 A cells (ATCC, USA) were cultured in RPMI-1640 or McCoy’s 5 A (Invitrogen, USA) medium supplemented with 10% fetal bovine serum (FBS; GIBCO, USA).

    Techniques: Protein-Protein interactions, Staining

    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