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trfs green  (MedChemExpress)


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    Structured Review

    MedChemExpress trfs green
    TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM <t>of</t> <t>TRFS-green</t> for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.
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    Images

    1) Product Images from "Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy"

    Article Title: Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy

    Journal: Redox Biology

    doi: 10.1016/j.redox.2025.103980

    TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM of TRFS-green for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.
    Figure Legend Snippet: TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM of TRFS-green for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.

    Techniques Used: Control, Incubation, Inverted Microscopy, Activity Assay, Transfection, Cell Cycle Assay, Flow Cytometry



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    TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM <t>of</t> <t>TRFS-green</t> for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.
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    Image Search Results


    TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM of TRFS-green for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.

    Journal: Redox Biology

    Article Title: Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy

    doi: 10.1016/j.redox.2025.103980

    Figure Lengend Snippet: TXNRD(i)s inhibit TXNRD1 and TXNRD2 enzymes and both enzymes are critical for growth of TNBC cells. A. HCC1806 cells were pretreated with 8VP101 or vehicle control for 1 h, then treated with 10 μM of TRFS-green for 4 h, followed by incubation with MitoTracker-red. Live cells were imaged on a Nikon Ti2E inverted microscope at 20x. Representative images shown. Cytosolic and mitochondrial TXNRD activity on average intensity per cell per field basis was quantified for 4 μM 8VP101 treatment. Average intensity was calculated from n = 3 biological replicates and n = 9 technical replicates. ∗∗∗∗p ≤ 0.0001. B. MDA-MB-231, HCC1806 and MCF-10A cells were transfected with siNeg, siTXNRD1, siTXNRD2, or both siTXNRD1 and siTXNRD2, 10 nM each, and monitored for cell growth every 12 h over 120 h using BioTek BioSpa. Data is shown as fold change normalized to the initial timepoint. Growth curves are averages −/+ sem from n = 3 biological replicates. End-point statistical significance was determined. ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.001; ∗∗∗∗p ≤ 0.0001. C. MDA-MB-231 cells were treated with DMSO, 8VP101 or 9VP19 at 10 μM each and monitored for cells growth as in (B). End-point statistical significance was determined. ∗∗∗∗p ≤ 0.0001. D. Cell cycle analysis using PI by flow cytometry of MDA-MB-231 cells. Cells were transfected with 10 nM siTXNRD1, 10 nM siTXNRD2, or a combination of 10 nM siTXNRD1 and 10 nM siTXNRD2 for 24 h. Statistical significance was determined by Kruskal-Wallis test followed by Dunns test comparing siTXNRD1, siTXNRD2, and both siTXNRD1 and siTXNRD2 to siNeg control. Data is presented as the mean±sem. ∗p ≤ 0.05; ns: not significant.

    Article Snippet: TRFS-green (HY-115640) was purchased from MedChemExpress.

    Techniques: Control, Incubation, Inverted Microscopy, Activity Assay, Transfection, Cell Cycle Assay, Flow Cytometry