spectrum analysis flow cytometry Search Results


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Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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New Brunswick Scientific 239 stable isotope analyses 240 continuous flow isotope ratio mass spectrometry
Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow <t>cytometry</t> showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.
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Figure 3. In vitro stability and cytotoxicity of M-TDH. (a) Tyndall effect showed good stability of M-TDH in saline with 10% FBS. (b) Cell viability after 24 h of incubation with PBS, TDH, M-TDH, and MnCl2, detected by CCK-8. (c, d) Cell apoptosis rates of DTC cells detected by flow <t>cytometry.</t> (e, f) Live/dead cell staining images and corresponding quantitative comparison of TPC1 and K1 cells after various treatments (scale bar 100 μm). (g, h) Hematological parameters of M-TDH detected by hemolysis experiments and corresponding quantitative measurements.
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Image Search Results


Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.

Journal: Cell death & disease

Article Title: Circular RNA TFRC/SCD1 mRNA interaction regulates ferroptosis and metastasis in gastric cancer.

doi: 10.1038/s41419-025-07759-x

Figure Lengend Snippet: Fig. 4 CircTFRC knockdown promoted the ferroptosis of GC cells. A, B Propidium iodide (PI) staining showing the cell death rates of control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). C, D Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). ROS reactive oxygen species. E, F ELISA assays showing the relative MDA levels in control (si-NC) and circTFRC knockdown (si-circTFRC) AGS and HGC-27 cells in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). MDA malondialdehyde. G, H Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.25 μM, 72 h). I, J Transwell assay evaluating the migration ability of AGS cells under control conditions (sh-NC) or with circTFRC knockdown (sh-circTFRC) in the absence or presence of ferrostatin-1 (0.75 μM, 16 h). K PI staining showing the cell death rates of control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. L Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. M Confocal microscopy showing the lipid ROS levels in control (sh-NC) and circTFRC knockdown (sh-circTFRC) AGS cells following treatment with RSL3 (1 μM) in the absence or presence of ferrostatin-1 (0.75 μM) for 16 h. Lipid ROS are stained with C11 BODIPY 581/591 probe (green). Nuclei are counterstained with DAPI (blue). Scale bar, 10 µm. Data are presented as mean ± SD. P-values were calculated using a two-tailed one-way ANOVA (A–F) or unpaired Student’s t test (H, J–L); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S4.

Article Snippet: Quantitative analysis of PI-positive populations was subsequently conducted using the Cytek® Northern LightsTM-CLC (NL-CLC) full spectrum flow cytometry system (Cytek® Biosciences, USA), with a minimum of 10,000 cells analyzed per condition.

Techniques: Knockdown, Staining, Control, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Colony Assay, Transwell Assay, Migration, Confocal Microscopy, Two Tailed Test

Fig. 6 CircTFRC exerted an oncogenic effect via SCD1 in GC cells. A CCK-8 assay showing the proliferation of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection at indicated time points (0, 24, 48, and 72 h). B, C Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection over 10 days. D, E Transwell assay showing the migration of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection over 24 h. Scale bar, 100 µm. F PI staining showing the cell death rates of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. G Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. ROS reactive oxygen species. H ELISA assays showing the relative MDA levels of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. MAD malondialdehyde. The data are shown as the mean ± SD. The P values were determined by a two-tailed unpaired Student’s t test (C, E–H) or two-way ANOVA (A); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S7.

Journal: Cell death & disease

Article Title: Circular RNA TFRC/SCD1 mRNA interaction regulates ferroptosis and metastasis in gastric cancer.

doi: 10.1038/s41419-025-07759-x

Figure Lengend Snippet: Fig. 6 CircTFRC exerted an oncogenic effect via SCD1 in GC cells. A CCK-8 assay showing the proliferation of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection at indicated time points (0, 24, 48, and 72 h). B, C Plate colony formation assay assessing colony formation in AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection over 10 days. D, E Transwell assay showing the migration of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection over 24 h. Scale bar, 100 µm. F PI staining showing the cell death rates of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. G Flow cytometry showing the lipid ROS levels (stained with C11 BODIPY 581/591) of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. ROS reactive oxygen species. H ELISA assays showing the relative MDA levels of AGS cells under control conditions (sh-NC), or upon circTFRC knockdown (sh-circTFRC) or sh-circTFRC + SCD1 vector cotransfection. MAD malondialdehyde. The data are shown as the mean ± SD. The P values were determined by a two-tailed unpaired Student’s t test (C, E–H) or two-way ANOVA (A); **P < 0.01, ***P < 0.001, ****P < 0.0001. See also Fig. S7.

Article Snippet: Quantitative analysis of PI-positive populations was subsequently conducted using the Cytek® Northern LightsTM-CLC (NL-CLC) full spectrum flow cytometry system (Cytek® Biosciences, USA), with a minimum of 10,000 cells analyzed per condition.

Techniques: CCK-8 Assay, Control, Knockdown, Plasmid Preparation, Cotransfection, Colony Assay, Transwell Assay, Migration, Staining, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Two Tailed Test

Figure 3. In vitro stability and cytotoxicity of M-TDH. (a) Tyndall effect showed good stability of M-TDH in saline with 10% FBS. (b) Cell viability after 24 h of incubation with PBS, TDH, M-TDH, and MnCl2, detected by CCK-8. (c, d) Cell apoptosis rates of DTC cells detected by flow cytometry. (e, f) Live/dead cell staining images and corresponding quantitative comparison of TPC1 and K1 cells after various treatments (scale bar 100 μm). (g, h) Hematological parameters of M-TDH detected by hemolysis experiments and corresponding quantitative measurements.

Journal: ACS applied materials & interfaces

Article Title: Manganese-Loaded pH-Responsive DNA Hydrogels Enable Tg-Guided Thyroid Tumor Targeted Magnetic Resonance Imaging.

doi: 10.1021/acsami.4c19676

Figure Lengend Snippet: Figure 3. In vitro stability and cytotoxicity of M-TDH. (a) Tyndall effect showed good stability of M-TDH in saline with 10% FBS. (b) Cell viability after 24 h of incubation with PBS, TDH, M-TDH, and MnCl2, detected by CCK-8. (c, d) Cell apoptosis rates of DTC cells detected by flow cytometry. (e, f) Live/dead cell staining images and corresponding quantitative comparison of TPC1 and K1 cells after various treatments (scale bar 100 μm). (g, h) Hematological parameters of M-TDH detected by hemolysis experiments and corresponding quantitative measurements.

Article Snippet: The quantification of cellular uptake was obtained by full spectrum analysis flow cytometry (ID7000 Sony, Japan).

Techniques: In Vitro, Saline, Incubation, CCK-8 Assay, Flow Cytometry, Staining, Comparison

Figure 5. Uptake efficiency and aptamer-mediated combination. (a, b) The uptake efficiency of M-TDH or TDH by K1 and TPC-1 cells detected by flow cytometry. (c) The in situ targeting of the nanohydrogel in frozen thyroid tissue sections. The white box shows the enlarged area, Cy5- TDH shows a red fluorescence signal, and a green fluorescence signal indicates the Tg distribution. (d) Nucleic acid−protein binding assay used to compare the combination between DH or TDH and endogenous Tg protein in the cellular environment.

Journal: ACS applied materials & interfaces

Article Title: Manganese-Loaded pH-Responsive DNA Hydrogels Enable Tg-Guided Thyroid Tumor Targeted Magnetic Resonance Imaging.

doi: 10.1021/acsami.4c19676

Figure Lengend Snippet: Figure 5. Uptake efficiency and aptamer-mediated combination. (a, b) The uptake efficiency of M-TDH or TDH by K1 and TPC-1 cells detected by flow cytometry. (c) The in situ targeting of the nanohydrogel in frozen thyroid tissue sections. The white box shows the enlarged area, Cy5- TDH shows a red fluorescence signal, and a green fluorescence signal indicates the Tg distribution. (d) Nucleic acid−protein binding assay used to compare the combination between DH or TDH and endogenous Tg protein in the cellular environment.

Article Snippet: The quantification of cellular uptake was obtained by full spectrum analysis flow cytometry (ID7000 Sony, Japan).

Techniques: Flow Cytometry, In Situ, Fluorescence, Protein Binding