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: Bioactive Materials

Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

doi: 10.1016/j.bioactmat.2026.01.004

Figure Lengend Snippet: LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

Techniques: Immunofluorescence, Staining, Quantitative RT-PCR, Inhibition

Journal: International Journal of Oncology

Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

doi: 10.3892/ijo.2026.5861

Figure Lengend Snippet: Effect of Topo II inhibitors on DNA damage formation and activation of DDR-related mechanisms in A2780 and A2780ADR cells. (A) At 24 h after treatment of logarithmically growing cells with the indicated concentrations of Doxo or Eto, the number of nuclear γH2AX-foci, 53BP1-foci, γH2AX/53BP1 co-localized foci and γH2AX pan-stained cells was analyzed. The upper part of the figure shows representative images (total magnification, ×1,000). Quantitative data depicted in the histogram are the mean ± SD from n=3 independent experiments with each five images being analyzed per experimental condition. * P≤0.05; ** P≤0.01; *** P≤0.001 (A2780 vs. A2780ADR); # P≤0.05; ## P≤0.01; ### P≤0.001 (treated vs. untreated control). Control experiments performed by use of 1st or 2nd antibody only or no antibody at all did not interfere with the signal of main interest (that is, nuclear foci; data not shown). (B) Logarithmically growing cells were treated with the indicated concentrations of Doxo for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting using EKR2 protein expression as loading control. Doxo, doxorubicin; Eto, etoposide; p-, phosphorylated; Chk1/2, checkpoint kinase 1/2; ERK2, extracellular regulated kinase; γH2AX, Ser139 phosphorylated histone H2AX; 2; Kap1, KRAB-associated protein 1; PARP, poly (ADP-ribose) polymerase; p21, cyclin-dependent kinase inhibitor 1; p53, tumor suppressor p53.

Article Snippet: The following primary antibodies were used: ATP7A (cat. no. PA5-103110; Invitrogen; Thermo Fisher Scientific; Inc.), Caspase-7 cleaved (Asp198; cat. no. 9491S; Cell Signaling Technology, Inc.), Chk1phospho (Ser345; cat. no. 2341, Cell Signaling Technology, Inc.), Chk2phosphoT68 (Y171; cat. no. ab32148; Abcam), CTR1/SLC31A1 (EPR7936; cat. no. ab129067; Abcam), Cyclin B1 (cat. no. 4138, Cell Signaling Technology, Inc.), ERK2 [PA5-32396, Invitrogen/Thermo Fisher Scientific; Carlsbad, USA], Galactosidase beta (E2U2I) (cat. no. 27198, Cell Signaling Technology, Inc.), GAPDH (14C10; cat. no. 2118S; Cell Signaling Technology, Inc.), H2AX phospho (Ser139, cloneJBW301; cat. no. 05-636, Merck KGaA), MDR1/ABCB1 (D3H1Q; cat. no. 12683; Cell Signaling Technology, Inc.), OCT2 (cat. no. MBS9600162, Biozol Diagnostics Vertrieb GmbH), P16 (F-12; cat. no. sc-1661; Santa Cruz Biotechnology, Inc.), p21 (C-19; cat. no. sc-397; Santa Cruz Biotechnology, Inc.), P53 phospho (S15; cat. no. 9284S; Cell Signaling Technology, Inc.), PARP (cat. no. 9542S, Cell Signaling Technology, Inc.), Rad51 (cat. no. ab63801; Abcam), RPA32 phospho (S4/S8; cat. no. ICH-00422; Bethyl Laboratories Inc.), TopBP1 (D8G4L; cat. no. 14342, Cell Signaling Technology, Inc.), Topoisomerase II alpha (D10G9; cat. no. 12286, Cell Signaling Technology, Inc.).

Techniques: Activation Assay, Staining, Control, Expressing, Western Blot

Journal: International Journal of Oncology

Article Title: Overcoming acquired doxorubicin resistance of ovarian carcinoma cells by verapamil-mediated promotion of DNA damage-driven cytotoxicity

doi: 10.3892/ijo.2026.5861

Figure Lengend Snippet: Influence of combined treatment of A2780ADR cells with Doxo and selected inhibitors on mechanism of the DDR and mRNA expression of selected susceptibility-related genes. (A) Logarithmically growing A2780ADR cells were co-treated with the indicated concentrations of Doxo and selected pharmacological inhibitors (concentrations see ) for 24 or 72 h. Afterwards, the protein expression of DDR-related factors was analyzed by western blotting. For loading control, blots were reprobed with ERK2 antibody. (B) Reverse transcription-quantitative PCR of the mRNA expression of selected factors known to contribute to different mechanisms of drug sensitivity. Data shown are mean ± SD from triplicate determinations as described in methods. Relative mRNA level in untreated A2780ADR cells was set to 1.0. Doxo, doxorubicin; DDR, DNA damage response; p-, phosphorylated; nd, not detectable; Bax, Bcl-2 associated protein X; Bcl-2, B-cell lymphoma; BBC3, Bcl-2 binding component 2; BRCA1, 2, breast cancer associated gene 1,2; Cl casp-7, cleaved caspase 7; Chk, checkpoint kinase; CXCL8, chemokine ligand 8 (interleukin 8); p21, CDK inhibitor 1; p16, CDK inhibitor 2; CDKN1A/2A, cyclin dependent kinae inhibitor 1A/2A; CCNB1, Cyclin B1; b-Gal, beta-galactosidase; FASL, FAS ligand; FASR, FAS receptor; GADD, growth arrest and DNA damage inducible GPX1, glutathione peroxidase 1; GSTM1, glutathione S-transferase 1; HMOX1, heme oxygenase 1; γH2AX, Ser139 phosphorylated histone H2AX; p53, tumor suppressor p53; PARP, poly (ADP-ribose) polymerase; PCNA-proliferating cell nuclear antigen; PGC1A, PPARG coactivator 1; PPARGC1A, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; RAD51, radiation damage gene 51; RPAreplication protein A; SOD1, superoxide dismutase 1; Ver, verapamil.

Article Snippet: The following primary antibodies were used: ATP7A (cat. no. PA5-103110; Invitrogen; Thermo Fisher Scientific; Inc.), Caspase-7 cleaved (Asp198; cat. no. 9491S; Cell Signaling Technology, Inc.), Chk1phospho (Ser345; cat. no. 2341, Cell Signaling Technology, Inc.), Chk2phosphoT68 (Y171; cat. no. ab32148; Abcam), CTR1/SLC31A1 (EPR7936; cat. no. ab129067; Abcam), Cyclin B1 (cat. no. 4138, Cell Signaling Technology, Inc.), ERK2 [PA5-32396, Invitrogen/Thermo Fisher Scientific; Carlsbad, USA], Galactosidase beta (E2U2I) (cat. no. 27198, Cell Signaling Technology, Inc.), GAPDH (14C10; cat. no. 2118S; Cell Signaling Technology, Inc.), H2AX phospho (Ser139, cloneJBW301; cat. no. 05-636, Merck KGaA), MDR1/ABCB1 (D3H1Q; cat. no. 12683; Cell Signaling Technology, Inc.), OCT2 (cat. no. MBS9600162, Biozol Diagnostics Vertrieb GmbH), P16 (F-12; cat. no. sc-1661; Santa Cruz Biotechnology, Inc.), p21 (C-19; cat. no. sc-397; Santa Cruz Biotechnology, Inc.), P53 phospho (S15; cat. no. 9284S; Cell Signaling Technology, Inc.), PARP (cat. no. 9542S, Cell Signaling Technology, Inc.), Rad51 (cat. no. ab63801; Abcam), RPA32 phospho (S4/S8; cat. no. ICH-00422; Bethyl Laboratories Inc.), TopBP1 (D8G4L; cat. no. 14342, Cell Signaling Technology, Inc.), Topoisomerase II alpha (D10G9; cat. no. 12286, Cell Signaling Technology, Inc.).

Techniques: Expressing, Western Blot, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Binding Assay