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In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; <t>(D)</t> <t>CCK-8</t> assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.
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In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; <t>(D)</t> <t>CCK-8</t> assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.
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In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; <t>(D)</t> <t>CCK-8</t> assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.
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In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; <t>(D)</t> <t>CCK-8</t> assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.
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Ferroptosis inducers cause cell death and affect PD-L1 expression, which can be inhibited by iron chelators. (A, B) A549 and H1299 cells were treated with erastin or RSL3 at different concentration gradients for 24 h, and cell viability was detected using <t>the</t> <t>CCK-8</t> kit. Subsequently, cells were co-treated with DFO (100 μM), ferrostatin-1 (2 μM), and the aforementioned ferroptosis inducers at different concentrations for another 24 h, with cell viability re-detected by CCK-8.(C) A549 and H1299 cells were treated with erastin (20 μM) and RSL3 (5 μM), respectively, for 0, 3, 6, 12, 18, and 24 h. PD-L1 expression was measured by qPCR.(D) After A549 and H1299 cells were treated with erastin (20 μM) for 24 h, they were further treated with DFO (100 μM) and ferrostatin-1 (2 μM) alone or in combination. PD-L1 expression in cells was then detected. (E) A549 and H1299 cells were treated with erastin (20 μM) for 24 h, and intracellular ROS was detected by flow cytometry. CCK-8, cell counting kit-8; DFO, deferoxamine; qPCR, quantitative polymerase chain reaction; PD-L1, programmed death-ligand 1; ROS, reactive oxygen species. *** p < 0.001.
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In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; (D) CCK-8 assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Translational Oncology

Article Title: Construction and validation of golgi apparatus-related genes as predictors of the immune microenvironment and prognosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102714

Figure Lengend Snippet: In Vitro functional experiments of GDI1 . (A). Expression differences of GDI1 among the NCM460, HCT116, and HT29 cell lines; (B)Verification of siRNA efficiency in knocking down GDI1 ; (C) Wound healing assay following GDI1 knockdown; (D) CCK-8 assay after GDI1 knockdown; (E) Apoptosis assay in the HT29 cell line after GDI1 knockdown; (F) Apoptosis assay in the HCT116 cell line after GDI1 knockdown. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: A suspension of 5000 transfected cells in 100 μL was distributed into each well of a 96-well plate, accompanied by the addition of 10 μL of CCK-8 solution (MCE, HY-K0301).

Techniques: In Vitro, Functional Assay, Expressing, Wound Healing Assay, Knockdown, CCK-8 Assay, Apoptosis Assay

Ferroptosis inducers cause cell death and affect PD-L1 expression, which can be inhibited by iron chelators. (A, B) A549 and H1299 cells were treated with erastin or RSL3 at different concentration gradients for 24 h, and cell viability was detected using the CCK-8 kit. Subsequently, cells were co-treated with DFO (100 μM), ferrostatin-1 (2 μM), and the aforementioned ferroptosis inducers at different concentrations for another 24 h, with cell viability re-detected by CCK-8.(C) A549 and H1299 cells were treated with erastin (20 μM) and RSL3 (5 μM), respectively, for 0, 3, 6, 12, 18, and 24 h. PD-L1 expression was measured by qPCR.(D) After A549 and H1299 cells were treated with erastin (20 μM) for 24 h, they were further treated with DFO (100 μM) and ferrostatin-1 (2 μM) alone or in combination. PD-L1 expression in cells was then detected. (E) A549 and H1299 cells were treated with erastin (20 μM) for 24 h, and intracellular ROS was detected by flow cytometry. CCK-8, cell counting kit-8; DFO, deferoxamine; qPCR, quantitative polymerase chain reaction; PD-L1, programmed death-ligand 1; ROS, reactive oxygen species. *** p < 0.001.

Journal: Translational Oncology

Article Title: Ferroptosis induction enhances anti-PD-1 efficacy in NSCLC via HIF-1α/PD-L1 modulation

doi: 10.1016/j.tranon.2026.102685

Figure Lengend Snippet: Ferroptosis inducers cause cell death and affect PD-L1 expression, which can be inhibited by iron chelators. (A, B) A549 and H1299 cells were treated with erastin or RSL3 at different concentration gradients for 24 h, and cell viability was detected using the CCK-8 kit. Subsequently, cells were co-treated with DFO (100 μM), ferrostatin-1 (2 μM), and the aforementioned ferroptosis inducers at different concentrations for another 24 h, with cell viability re-detected by CCK-8.(C) A549 and H1299 cells were treated with erastin (20 μM) and RSL3 (5 μM), respectively, for 0, 3, 6, 12, 18, and 24 h. PD-L1 expression was measured by qPCR.(D) After A549 and H1299 cells were treated with erastin (20 μM) for 24 h, they were further treated with DFO (100 μM) and ferrostatin-1 (2 μM) alone or in combination. PD-L1 expression in cells was then detected. (E) A549 and H1299 cells were treated with erastin (20 μM) for 24 h, and intracellular ROS was detected by flow cytometry. CCK-8, cell counting kit-8; DFO, deferoxamine; qPCR, quantitative polymerase chain reaction; PD-L1, programmed death-ligand 1; ROS, reactive oxygen species. *** p < 0.001.

Article Snippet: Reagents and Antibodies Cell culture media and reagents: Ham's F-12 K, DMEM, RPMI-1640 (Servicebio), BCA protein assay kit, CCK-8 kit, RIPA lysis buffer (Servicebio), Lovastatin, Fluvastatin, RSL3, Erastin (MCE), deferoxamine mesylate, and Ferrostatin-1 (MCE).

Techniques: Expressing, Concentration Assay, CCK-8 Assay, Flow Cytometry, Cell Counting, Real-time Polymerase Chain Reaction