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ATCC ec cell lines kle

ATP-based viability assays under DOX treatment. <t>(A)</t> <t>AN3CA</t> cells were exposed to increasing DOX concentrations (0.125–4 µM). The ATPlite assay revealed a dose-dependent reduction in viability, evident from 0.5 µM. (B) <t>KLE</t> cells treated with DOX (0.125–4 µM) displayed a moderate but non–dose-dependent reduction in viability. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; ***p < 0.0005 ****p < 0.0001.

Ec Cell Lines Kle, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 461 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione"

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

Journal: Frontiers in Physiology

doi: 10.3389/fphys.2026.1733194

ATP-based viability assays under DOX treatment. (A) AN3CA cells were exposed to increasing DOX concentrations (0.125–4 µM). The ATPlite assay revealed a dose-dependent reduction in viability, evident from 0.5 µM. (B) KLE cells treated with DOX (0.125–4 µM) displayed a moderate but non–dose-dependent reduction in viability. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; ***p < 0.0005 ****p < 0.0001.

Figure Legend Snippet: ATP-based viability assays under DOX treatment. (A) AN3CA cells were exposed to increasing DOX concentrations (0.125–4 µM). The ATPlite assay revealed a dose-dependent reduction in viability, evident from 0.5 µM. (B) KLE cells treated with DOX (0.125–4 µM) displayed a moderate but non–dose-dependent reduction in viability. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; ***p < 0.0005 ****p < 0.0001.

Techniques Used: Control

ATP-based viability assays under menadione treatment. (A) AN3CA cells were exposed to menadione (1–25 µM). The ATPlite assay showed strong cytotoxic effects at 25 µM. (B) KLE cells treated with menadione (1–25 µM) also exhibited markedly reduced viability at 25 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. ****p < 0.0001.

Figure Legend Snippet: ATP-based viability assays under menadione treatment. (A) AN3CA cells were exposed to menadione (1–25 µM). The ATPlite assay showed strong cytotoxic effects at 25 µM. (B) KLE cells treated with menadione (1–25 µM) also exhibited markedly reduced viability at 25 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. ****p < 0.0001.

Techniques Used: Control

ROS generation induced by DOX in EC cell lines. (A) AN3CA cells were exposed to DOX (0.125–4 µM) for 24 h. ROS levels, measured using the CellROX® assay, were significantly elevated at 2 μM and 4 µM. (B) KLE cells treated under the same conditions showed a slight increase in ROS at 2 μM and 4 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; **p < 0.005.

Figure Legend Snippet: ROS generation induced by DOX in EC cell lines. (A) AN3CA cells were exposed to DOX (0.125–4 µM) for 24 h. ROS levels, measured using the CellROX® assay, were significantly elevated at 2 μM and 4 µM. (B) KLE cells treated under the same conditions showed a slight increase in ROS at 2 μM and 4 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; **p < 0.005.

Techniques Used: Control

ROS generation induced by menadione in EC cell lines. (A) AN3CA cells treated with menadione (1–25 µM) for 24 h displayed a significant ROS increase at 10 µM. (B) In KLE cells, ROS elevation remained marginal and did not reach statistical significance across tested doses. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05.

Figure Legend Snippet: ROS generation induced by menadione in EC cell lines. (A) AN3CA cells treated with menadione (1–25 µM) for 24 h displayed a significant ROS increase at 10 µM. (B) In KLE cells, ROS elevation remained marginal and did not reach statistical significance across tested doses. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05.

Techniques Used: Control

Validation of primary antibodies against SESN2, SESN3, and SOD1 using ICW assay. (A) AN3CA and KLE cells were probed with anti-SESN2 antibody (dilutions 1:1200–1:150). (B) AN3CA and KLE cells were probed with anti-SESN3 antibody (dilutions 1:1000–1:100). (C) AN3CA and KLE cells were probed with anti-SOD1 antibody (dilutions 1:1000–1:100). Secondary antibodies (1:800, LI-COR) were applied, with CellTag™ 520 (1:500, LI-COR) as a loading control for signal normalization. Data are shown as mean ± SD of three technical replicate wells from a single antibody-optimization experiment. Statistical significance was assessed by two-way ANOVA (factors: cell line and antibody dilution), followed by Sidak’s multiple-comparisons test comparing AN3CA vs. KLE within each dilution. **p < 0.005.

Figure Legend Snippet: Validation of primary antibodies against SESN2, SESN3, and SOD1 using ICW assay. (A) AN3CA and KLE cells were probed with anti-SESN2 antibody (dilutions 1:1200–1:150). (B) AN3CA and KLE cells were probed with anti-SESN3 antibody (dilutions 1:1000–1:100). (C) AN3CA and KLE cells were probed with anti-SOD1 antibody (dilutions 1:1000–1:100). Secondary antibodies (1:800, LI-COR) were applied, with CellTag™ 520 (1:500, LI-COR) as a loading control for signal normalization. Data are shown as mean ± SD of three technical replicate wells from a single antibody-optimization experiment. Statistical significance was assessed by two-way ANOVA (factors: cell line and antibody dilution), followed by Sidak’s multiple-comparisons test comparing AN3CA vs. KLE within each dilution. **p < 0.005.

Techniques Used: Biomarker Discovery, Control

Differential effects of DOX and menadione on SOD1 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced an upward trend in normalized SOD1 levels. (B) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SOD1 levels at 1–10 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), normalized SOD1 levels remained relatively stable at lower concentrations (0.25–0.5 µM) but declined markedly from 1 µM onward. (F) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced dose-dependent modulation of SOD1 protein levels. (H) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SOD1/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; ***p < 0.0005; ****p < 0.0001.

Figure Legend Snippet: Differential effects of DOX and menadione on SOD1 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced an upward trend in normalized SOD1 levels. (B) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SOD1 levels at 1–10 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), normalized SOD1 levels remained relatively stable at lower concentrations (0.25–0.5 µM) but declined markedly from 1 µM onward. (F) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced dose-dependent modulation of SOD1 protein levels. (H) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SOD1/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; ***p < 0.0005; ****p < 0.0001.

Techniques Used: Expressing, Fluorescence, Control

Differential effects of DOX and menadione on SESN2 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced a modest upward trend in normalized SESN2 levels. (B) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SESN2 levels at 1–5 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), SESN2 exhibited a biphasic response, peaking at 0.125 µM and declining sharply from 1 µM onward. (F) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN2 upregulation at 0.125–0.25 µM, followed by progressive downregulation with the lowest levels at 4 µM. (H) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN2/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005; ***p < 0.0005.

Figure Legend Snippet: Differential effects of DOX and menadione on SESN2 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced a modest upward trend in normalized SESN2 levels. (B) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SESN2 levels at 1–5 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), SESN2 exhibited a biphasic response, peaking at 0.125 µM and declining sharply from 1 µM onward. (F) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN2 upregulation at 0.125–0.25 µM, followed by progressive downregulation with the lowest levels at 4 µM. (H) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN2/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005; ***p < 0.0005.

Techniques Used: Expressing, Fluorescence, Control

Differential effects of DOX and menadione on SESN3 expression in AN3CA and KLE cells assessed by ICW assay. (A) In KLE cells, menadione (1–25 µM) strongly induced SESN3 in a dose-dependent manner at 1–10 μM, followed by a marked decrease at 25 µM. (B) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (C) In AN3CA cells, menadione produced a modest and stable SESN3 response without reaching statistical significance. (D) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells exposed to DOX (0.125–4 µM), SESN3 exhibited a biphasic response, peaking at 0.25 µM and declining sharply from 0.5 µM onward. (F) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN3 upregulation at 0.125–0.25 µM, followed by gradual reduction at higher concentrations. (H) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN3/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005.

Figure Legend Snippet: Differential effects of DOX and menadione on SESN3 expression in AN3CA and KLE cells assessed by ICW assay. (A) In KLE cells, menadione (1–25 µM) strongly induced SESN3 in a dose-dependent manner at 1–10 μM, followed by a marked decrease at 25 µM. (B) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (C) In AN3CA cells, menadione produced a modest and stable SESN3 response without reaching statistical significance. (D) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells exposed to DOX (0.125–4 µM), SESN3 exhibited a biphasic response, peaking at 0.25 µM and declining sharply from 0.5 µM onward. (F) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN3 upregulation at 0.125–0.25 µM, followed by gradual reduction at higher concentrations. (H) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN3/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005.

Techniques Used: Expressing, Fluorescence, Produced, Control

SESN2, SESN3, and SOD1 gene expression profiles in AN3CA and KLE cells analyzed by qRT-PCR. (A) SESN2 mRNA was significantly upregulated in both cell lines following 4 µM DOX treatment. Menadione induced robust SESN2 upregulation at 25 µM in KLE cells. (B) SESN3 mRNA was strongly upregulated by DOX in both lines, whereas menadione downregulated SESN3 in both cell lines. (C) SOD1 mRNA showed significant upregulation in KLE cells under 4 µM DOX, while AN3CA cells exhibited no significant changes. Under menadione, AN3CA cells displayed significant downregulation of SOD1 at 10 µM and 25 μM, while KLE cells showed downregulation at 25 µM. RT–qPCR data were normalized to UBC as the endogenous reference gene and are presented relative to the untreated control (medium-only). Each condition was analyzed in three technical replicate wells. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. Key findings were confirmed in an independent repeat experiment. *p < 0.05; **p < 0.005; ***p < 0.0005.

Figure Legend Snippet: SESN2, SESN3, and SOD1 gene expression profiles in AN3CA and KLE cells analyzed by qRT-PCR. (A) SESN2 mRNA was significantly upregulated in both cell lines following 4 µM DOX treatment. Menadione induced robust SESN2 upregulation at 25 µM in KLE cells. (B) SESN3 mRNA was strongly upregulated by DOX in both lines, whereas menadione downregulated SESN3 in both cell lines. (C) SOD1 mRNA showed significant upregulation in KLE cells under 4 µM DOX, while AN3CA cells exhibited no significant changes. Under menadione, AN3CA cells displayed significant downregulation of SOD1 at 10 µM and 25 μM, while KLE cells showed downregulation at 25 µM. RT–qPCR data were normalized to UBC as the endogenous reference gene and are presented relative to the untreated control (medium-only). Each condition was analyzed in three technical replicate wells. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. Key findings were confirmed in an independent repeat experiment. *p < 0.05; **p < 0.005; ***p < 0.0005.

Techniques Used: Gene Expression, Quantitative RT-PCR, Control

Image Search Results

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: ATP-based viability assays under DOX treatment. (A) AN3CA cells were exposed to increasing DOX concentrations (0.125–4 µM). The ATPlite assay revealed a dose-dependent reduction in viability, evident from 0.5 µM. (B) KLE cells treated with DOX (0.125–4 µM) displayed a moderate but non–dose-dependent reduction in viability. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; ***p < 0.0005 ****p < 0.0001.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: ATP-based viability assays under menadione treatment. (A) AN3CA cells were exposed to menadione (1–25 µM). The ATPlite assay showed strong cytotoxic effects at 25 µM. (B) KLE cells treated with menadione (1–25 µM) also exhibited markedly reduced viability at 25 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. ****p < 0.0001.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: ROS generation induced by DOX in EC cell lines. (A) AN3CA cells were exposed to DOX (0.125–4 µM) for 24 h. ROS levels, measured using the CellROX® assay, were significantly elevated at 2 μM and 4 µM. (B) KLE cells treated under the same conditions showed a slight increase in ROS at 2 μM and 4 µM. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05; **p < 0.005.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: ROS generation induced by menadione in EC cell lines. (A) AN3CA cells treated with menadione (1–25 µM) for 24 h displayed a significant ROS increase at 10 µM. (B) In KLE cells, ROS elevation remained marginal and did not reach statistical significance across tested doses. Data are shown as mean ± SD of six technical replicate wells per condition. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control (medium-only). Vehicle control (DMSO) was included and showed no significant difference vs. untreated control. Experiments were repeated independently twice with consistent results. *p < 0.05.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: Validation of primary antibodies against SESN2, SESN3, and SOD1 using ICW assay. (A) AN3CA and KLE cells were probed with anti-SESN2 antibody (dilutions 1:1200–1:150). (B) AN3CA and KLE cells were probed with anti-SESN3 antibody (dilutions 1:1000–1:100). (C) AN3CA and KLE cells were probed with anti-SOD1 antibody (dilutions 1:1000–1:100). Secondary antibodies (1:800, LI-COR) were applied, with CellTag™ 520 (1:500, LI-COR) as a loading control for signal normalization. Data are shown as mean ± SD of three technical replicate wells from a single antibody-optimization experiment. Statistical significance was assessed by two-way ANOVA (factors: cell line and antibody dilution), followed by Sidak’s multiple-comparisons test comparing AN3CA vs. KLE within each dilution. **p < 0.005.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Biomarker Discovery, Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: Differential effects of DOX and menadione on SOD1 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced an upward trend in normalized SOD1 levels. (B) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SOD1 levels at 1–10 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), normalized SOD1 levels remained relatively stable at lower concentrations (0.25–0.5 µM) but declined markedly from 1 µM onward. (F) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced dose-dependent modulation of SOD1 protein levels. (H) Raw fluorescence signals corresponding to SOD1 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SOD1/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; ***p < 0.0005; ****p < 0.0001.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Expressing, Fluorescence, Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: Differential effects of DOX and menadione on SESN2 expression in AN3CA and KLE cells assessed by ICW assay. (A) In AN3CA cells, menadione (1–25 µM) induced a modest upward trend in normalized SESN2 levels. (B) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (C) In KLE cells, menadione increased normalized SESN2 levels at 1–5 μM, followed by a marked decrease at 25 µM. (D) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells treated with DOX (0.125–4 µM), SESN2 exhibited a biphasic response, peaking at 0.125 µM and declining sharply from 1 µM onward. (F) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN2 upregulation at 0.125–0.25 µM, followed by progressive downregulation with the lowest levels at 4 µM. (H) Raw fluorescence signals corresponding to SESN2 (700 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN2/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005; ***p < 0.0005.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Expressing, Fluorescence, Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: Differential effects of DOX and menadione on SESN3 expression in AN3CA and KLE cells assessed by ICW assay. (A) In KLE cells, menadione (1–25 µM) strongly induced SESN3 in a dose-dependent manner at 1–10 μM, followed by a marked decrease at 25 µM. (B) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (C) In AN3CA cells, menadione produced a modest and stable SESN3 response without reaching statistical significance. (D) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (E) In AN3CA cells exposed to DOX (0.125–4 µM), SESN3 exhibited a biphasic response, peaking at 0.25 µM and declining sharply from 0.5 µM onward. (F) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). (G) In KLE cells, DOX induced modest SESN3 upregulation at 0.125–0.25 µM, followed by gradual reduction at higher concentrations. (H) Raw fluorescence signals corresponding to SESN3 (800 nm) and CellTag™ 520 (520 nm). Normalized protein levels were calculated as SESN3/CellTag™ 520 ratios (normalized signal). Untreated control (medium-only) wells were included in each experiment and served as the reference group for comparisons. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. For DOX, the figure shows a representative ICW run (n = 6 technical replicate wells per condition), and the experiment was repeated independently once with consistent results (n = 3). For menadione, data are from one ICW experiment (n = 6 technical replicate wells per condition). *p < 0.05; **p < 0.005.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Expressing, Fluorescence, Produced, Control

Journal: Frontiers in Physiology

Article Title: Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione

doi: 10.3389/fphys.2026.1733194

Figure Lengend Snippet: SESN2, SESN3, and SOD1 gene expression profiles in AN3CA and KLE cells analyzed by qRT-PCR. (A) SESN2 mRNA was significantly upregulated in both cell lines following 4 µM DOX treatment. Menadione induced robust SESN2 upregulation at 25 µM in KLE cells. (B) SESN3 mRNA was strongly upregulated by DOX in both lines, whereas menadione downregulated SESN3 in both cell lines. (C) SOD1 mRNA showed significant upregulation in KLE cells under 4 µM DOX, while AN3CA cells exhibited no significant changes. Under menadione, AN3CA cells displayed significant downregulation of SOD1 at 10 µM and 25 μM, while KLE cells showed downregulation at 25 µM. RT–qPCR data were normalized to UBC as the endogenous reference gene and are presented relative to the untreated control (medium-only). Each condition was analyzed in three technical replicate wells. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test comparing each treatment condition to the untreated control. Key findings were confirmed in an independent repeat experiment. *p < 0.05; **p < 0.005; ***p < 0.0005.

Article Snippet: The EC cell lines KLE (CRL-1622TM) and AN3CA (HTB-111TM) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, United States).

Techniques: Gene Expression, Quantitative RT-PCR, Control

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