Journal: Clinical and Translational Radiation Oncology

Article Title: MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53

doi: 10.1016/j.ctro.2026.101147

Figure Lengend Snippet: Different protein expression of p-ATM, p- p 53 and p53 in breast cancer cells treated with combination of monoHER (M) and radiation (RT). Representative Western blots of p-ATM, p-p53 and p53 in MCF7 (A), T47D (E) and MCF10A (H) cells. Quantification of p-ATM (B), p-p53 (C) and p53 (D) protein expression in MCF7 cells. Quantification of p-ATM (E), p-p53 (F) and p53 (G) protein expression in T47D cells. Quantification of p-ATM (I), p-p53 (J) and p53 (K) protein expression in MCF10A cells. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01.

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST for 1 h at RT and incubated overnight at 4°C with primary antibodies against p-ATM (1:2000; Cell Signaling Technology, 5883), p-p53 (1:1000; Cell Signaling Technology, 9284) and p53 (1:1000; Cell Signaling Technology, 9282). α-Tubulin (1:1000, Sigma Aldrich, T7451) or Vinculin (1:1000, Sigma Aldrich, V9131) were used as loading controls.

Techniques: Expressing, Western Blot

Journal: Clinical and Translational Radiation Oncology

Article Title: MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53

doi: 10.1016/j.ctro.2026.101147

Figure Lengend Snippet: Monoher interacts with p53. Biomolecular interactions of monoHER with wild-type p53 (A) and mutant p53 (B). Docking scores are indicated at the bottom of the image. Representative Western blots and quantification (E) of the CETSA experiment with cell lysates of MCF7 cells, which were treated with DMEM (C) or monoHER (D). Data are presented as mean ± SEM from three independent experiments.

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST for 1 h at RT and incubated overnight at 4°C with primary antibodies against p-ATM (1:2000; Cell Signaling Technology, 5883), p-p53 (1:1000; Cell Signaling Technology, 9284) and p53 (1:1000; Cell Signaling Technology, 9282). α-Tubulin (1:1000, Sigma Aldrich, T7451) or Vinculin (1:1000, Sigma Aldrich, V9131) were used as loading controls.

Techniques: Mutagenesis, Western Blot

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

Article Snippet: The primary antibodies included phosphorylated STAT3 (Tyr705) (p-STAT3; Abcam, #ab308386; 1:1000), cyclin G1 (CCNG1; Santa Cruz Biotechnology, #sc-8016; 1:1000), γH2AX (Abcam, #ab81299; 1:5000), TP53 (Cell Signaling Technology, #32532; 1:1000), and GAPDH (Abcam, #ab8245; 1:10000) antibodies.

Techniques: Transfection, Plasmid Preparation, Cell Culture, Irradiation, Flow Cytometry, Western Blot, Expressing, Isolation

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

Article Snippet: The primary antibodies included phosphorylated STAT3 (Tyr705) (p-STAT3; Abcam, #ab308386; 1:1000), cyclin G1 (CCNG1; Santa Cruz Biotechnology, #sc-8016; 1:1000), γH2AX (Abcam, #ab81299; 1:5000), TP53 (Cell Signaling Technology, #32532; 1:1000), and GAPDH (Abcam, #ab8245; 1:10000) antibodies.

Techniques: Irradiation, Phospho-proteomics, Ubiquitin Proteomics