Journal: bioRxiv

Article Title: Integrated stress response activation in combination PG3 and cisplatin-treated TP53 -mutated head and neck squamous carcinoma cells induces potent apoptotic response

doi: 10.64898/2026.09.22.752907

Figure Lengend Snippet: (A) sgControl PANC1, PANC1 HRI -/- #2, PANC1 PKR -/- #1, PANC1 PERKI -/- #1/2, and PANC1 GCN2 -/- #1/2 cells were treated with cisplatin for 16 hours, then a western blot assay was performed using the indicated antibodies. (B) sgControl PANC1, and PANC1 HRI -/- #2 cells were treated with cisplatin for 6 hours, then a western blot assay was performed using the indicated antibodies. (C) FaDu and (D) HT29 cells were transfected with Control or HRI siRNAs. After 24 hours, the FaDu and HT29 cells were treated with cisplatin or PG3 for 16 hours. Western blot analysis was performed using the indicated antibodies. (E) FaDu and (F) HT29 cells were transfected with Control or PERK siRNAs. After 24 hours’ transfection, the FaDu and HT29 cells were treated with cisplatin and TG for 15 or 21 hours, respectively. Western blot analysis was performed using the indicated antibodies.

Article Snippet: Antibodies for PUMA, CK1δ, and HRI were from Santa Cruz Biotechnology; for caspase-8, cleaved caspase-8, caspase-9, caspase-3, cleaved-caspase-3, PARP, cleaved-PARP, GFP, CDK2, p-CDK2(T160), Mcl-1, p-Mcl-1(S64), β-TrCP1, PERK, PKR, GCN2, eIF2α, p-eIF2α (Ser51), ATF3, and ATF4 were from Cell Signaling Technology.

Techniques: Western Blot, Transfection, Control, Analysis

Journal: Translational Lung Cancer Research

Article Title: Targeted dual-responsive nanocapsules for synergistic cisplatin and paclitaxel prodrug delivery in the treatment of lung cancer

doi: 10.21037/tlcr-2026-0967

Figure Lengend Snippet: PTX/Pt@RGD induces oxidative stress, mitochondrial dysfunction, DNA damage, and apoptosis in A549 cells. (A) PTX/Pt@RGD induced ROS generation in A549 cells. Representative fluorescence images of A549 cells stained with DCFH-DA after 24-h treatment with the indicated formulations (green fluorescence indicates ROS levels) (magnification: 20×). Quantitative analysis of relative DCFH-DA fluorescence intensity. Data are presented as the mean ± SD from three independent experiments (n=3). Statistical significance was determined via one-way ANOVA followed by the Tukey post hoc test. (B) PTX/Pt@RGD induced loss of mitochondrial membrane potential in A549 cells. Representative fluorescence images of A549 cells stained with JC-1 after 24-h treatment with the indicated formulations. JC-1 monomer emitted green fluorescence (Ex/Em = 490/530 nm), and JC-1 aggregates emitted red fluorescence (Ex/Em =490/590 nm) (magnification: ×20). Quantitative analysis of the red:green fluorescence intensity ratio. Data are presented as the mean ± SD from three independent experiments (n=3). Statistical significance was determined via one-way ANOVA followed by the Tukey post hoc test. (C) PTX/Pt@RGD induced DNA damage in A549 cells (γ-H2AX immunofluorescence). Representative immunofluorescence images of A549 cells stained with anti-γ-H2AX antibody (green) and DAPI (blue) after 24-h treatment with the indicated formulations (magnification: ×20). Quantitative analysis of relative DNA damage index (γ-H2AX/DAPI mean fluorescence intensity). Data are presented as the mean ± SD from three independent experiments (n=3). Statistical significance was determined via one-way ANOVA followed by the Tukey post hoc test. (D) Western blot analysis of apoptosis- and inflammation-related proteins in A549 cells after different treatments. Protein expression of Bax, Bcl-2, Caspase-9, and COX-2 was detected by Western blotting with β-actin as the loading control. Relative protein levels were quantified and normalized to β-actin. Data are shown as the mean ± SD (n=3). (E) PTX/Pt@RGD induced apoptosis in A549 cells. Flow cytometry analysis of apoptosis in A549 cells after treatment with control, PTX, Pt, PTX/Pt, or PTX/Pt@RGD. The bar graph shows the quantitative percentage of apoptotic cells. Data are presented as mean ± SD (n=3). ns, not significant; *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 compared to the control group. ANOVA, analysis of variance; Ex/Em, excitation/emission; Pt, cisplatin; PTX, paclitaxel; RGD, arginine-glycine-aspartic acid; ROS, reactive oxygen species; SD, standard deviation.

Article Snippet: Antibodies included primary antibodies against CD31 [cat. no. 11265-1-P; rabbit polyclonal antibody; Western blotting (WB) 1:500; immunohistochemistry (IHC) 1:100; Proteintech, Rosemont, IL, USA], Ki-67 (cat. no. 27309-1-AP; rabbit polyclonal antibody; IHC 1:200; Proteintech), PCNA (cat. no. 10205-2-AP; rabbit polyclonal antibody; IHC 1:500; Proteintech), Bcl-2 (cat. no. 12789-1-AP; WB 1:1,000; Proteintech), Caspase-9 (cat. no. 10380-1-AP; WB 1:1,000; Proteintech), Bax (cat. no. 50599-2-Ig; WB 1:2,000; Proteintech), COX-2 (cat. no. 12375-1-AP, WB 1:1000; Proteintech), and β-actin (cat. no. 66009-1-Ig; WB 1:5,000; internal control), as well as horseradish peroxidase (HRP)-conjugated goat anti-rabbit secondary antibody (cat. no. SA00001-2; WB 1:5,000; Proteintech).

Techniques: Fluorescence, Staining, Analysis, Membrane, Immunofluorescence, Western Blot, Expressing, Control, Flow Cytometry, Standard Deviation