Journal: Cancer Reports

Article Title: DKK1 Promotes Cisplatin Resistance in Oral Squamous Cell Carcinoma via SLC3A2 ‐Dependent Ferroptosis Suppression

doi: 10.1002/cnr2.70715

Figure Lengend Snippet: DKK1 regulates SLC3A2‐associated ferroptosis through the β‐catenin/STAT3 axis. (A‐D) Western blotting and RT‐qPCR analyses of pathway‐associated markers in CAL‐27‐CR (A, B) and SCC‐9‐CR (C, D) cells following DKK1 knockdown and/or treatment with the STAT3 inhibitor STAT3‐IN‐3 (1 μM, 24 h). (E) C11‐BODIPY 581/591 staining showing lipid peroxidation in CR cells following DKK1 knockdown and/or STAT3 inhibition. (F) FerroOrange staining showing intracellular Fe 2+ accumulation in CR cells following DKK1 knockdown and/or STAT3 inhibition. (G–I) Assessment of ferroptosis‐associated indicators, including ROS accumulation (G), GSH levels (H), and MDA production (I), in CR cells following DKK1 knockdown and/or STAT3 inhibition. (J) CCK‐8 cell viability assay showing the effects of DKK1 knockdown and/or STAT3 inhibition on cisplatin sensitivity in CR cells. Data are presented as the mean ± SD from three independent biological experiments unless otherwise indicated. Statistical significance was assessed using two‐tailed Student's t ‐test for two‐group comparisons or one‐way ANOVA followed by Tukey's post hoc test for multiple‐group comparisons. * p < 0.05, ** p < 0.01; ns, not significant.

Article Snippet: For STAT3 inhibition experiments, cells were treated with the STAT3 inhibitor STAT3‐IN‐3 (1 μM; cat. no. HY‐128588; MCE) for 24 h.

Techniques: Western Blot, Quantitative RT-PCR, Knockdown, Staining, Inhibition, CCK-8 Assay, Cell Viability Assay, Sensitivity, Two Tailed Test

Journal: Cancer Reports

Article Title: DKK1 Promotes Cisplatin Resistance in Oral Squamous Cell Carcinoma via SLC3A2 ‐Dependent Ferroptosis Suppression

doi: 10.1002/cnr2.70715

Figure Lengend Snippet: DKK1 depletion potentiates cisplatin efficacy against resistant OSCC xenografts in vivo. (A, B) Macroscopic appearance of excised tumors at day 27 post‐treatment (A) and the corresponding terminal tumor weights (B) across different cohorts. (C) Tumor volume growth trajectories in mice bearing CAL‐27‐CR xenografts subjected to different interventions. (D) Representative immunohistochemical (IHC) staining showing DKK1, β‐catenin, p‐STAT3, and SLC3A2 expression patterns in resected xenograft tissues. Scale bar = 100 μm. (E) Representative IHC staining of 4‐HNE in xenograft tissues, indicating lipid peroxidation in vivo. Scale bar = 50 μm. Data are presented as the mean ± SD; n = 6 mice per group. Statistical significance was assessed using one‐way ANOVA followed by Tukey's post hoc test for comparisons among multiple groups. Tumor growth curves were analyzed using repeated‐measures ANOVA. * p < 0.05, ** p < 0.01; ns, not significant.

Article Snippet: For STAT3 inhibition experiments, cells were treated with the STAT3 inhibitor STAT3‐IN‐3 (1 μM; cat. no. HY‐128588; MCE) for 24 h.

Techniques: In Vivo, Immunohistochemical staining, Immunohistochemistry, Expressing, Xenograft Assay

Journal: Cancer Reports

Article Title: DKK1 Promotes Cisplatin Resistance in Oral Squamous Cell Carcinoma via SLC3A2 ‐Dependent Ferroptosis Suppression

doi: 10.1002/cnr2.70715

Figure Lengend Snippet: Graphical abstract. DKK1 Confers Cisplatin Resistance in Oral Squamous Cell Carcinoma via WNT/β‐catenin/STAT3‐SLC3A2‐Mediated Ferroptosis Suppression.

Article Snippet: For STAT3 inhibition experiments, cells were treated with the STAT3 inhibitor STAT3‐IN‐3 (1 μM; cat. no. HY‐128588; MCE) for 24 h.

Techniques:

Journal: Communications Biology

Article Title: Ketogenic diet alleviates acute radiation-induced intestinal injury through JAK2/STAT3/RORγt/IL-17A signaling pathway via gut microbiome

doi: 10.1038/s42003-026-10546-9

Figure Lengend Snippet: A Western blot analysis of phosphorylated JAK2 (p-JAK2), STAT3 (p-STAT3), and RORγt in irradiated NCM460 cells treated with β-hydroxybutyrate (BHB) or high-salt (HS). B mRNA levels of IL-17A in irradiated NCM460 cells treated with BHB or HS. C ELISA assay to detect IL-17A levels in the supernatant of irradiated NCM460 cells following BHB or HS treatment. D Western blot analysis of RORγt expression in irradiated NCM460 cells following treatment with the STAT3 inhibitor (C188-9) or activator (Colivelin), combined with BHB or HS. E ELISA assay to detect IL-17A levels in irradiated NCM460 cells following STAT3 inhibitor (C188-9) or activator (Colivelin) treatment, combined with BHB or HS. F Western blot analysis confirming RORγt overexpression in NCM460 cells. G qRT-PCR analysis detecting the mRNA levels of the IL-17A gene after RORγt overexpression. H Dual-luciferase reporter assay to assess transcriptional activity of the IL-17A gene promoter in irradiated NCM460 cells treated with BHB or HS. I Predicted RORγt binding sites in the IL-17A gene promoter region. J Dual-luciferase reporter assay to detect transcriptional activity of the IL-17A gene promoter in RORγt-overexpressing NCM460 cells with wild-type or mutated binding sites. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: For drug intervention experiments, the Stat3 agonist Colivelin (MedChemExpress, USA) and the Stat3 inhibitor C188-9 (MedChemExpress, USA) were added to the medium following treatment with sodium chloride solution or BHB.

Techniques: Western Blot, Analysis, Irradiation, Enzyme-linked Immunosorbent Assay, Expressing, Over Expression, Quantitative RT-PCR, Luciferase, Activity Assay, Binding Assay