Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

Techniques: Concentration Assay, CRISPR

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

Techniques: Inhibition, Expressing, Control

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

Techniques: Inhibition

Journal: RSC Advances

Article Title: Comparative evaluation of donepezil-loaded polymeric and liposomal nanoparticles for Alzheimer's disease: biocompatibility, drug release kinetics, and cellular uptake study

doi: 10.1039/d6ra00929h

Figure Lengend Snippet: Effects of donepezil control solution, donepezil-loaded polymeric NPs, and donepezil-loaded DPPC-based liposomes treatment on ECV-304 and PC-12 cells. Cells were treated with increasing concentrations (3.125–50 µg mL −1 ) of each formulation in a time-dependent manner. All formulations maintained cell viability above 80% at concentrations up to 50 µg mL −1 in both cell lines, indicating acceptable biocompatibility. A Two-way ANOVA followed by Tukey's test was applied at each time point independently to compare the effect of different formulations across different concentrations within each cell line. **Significant with respect to the control ( p < 0.01), as shown by two-way ANOVA. The data is reported as mean ± SEM ( n = 3).

Article Snippet: The human endothelial-like cell line ECV-304 and the immortalized rat-derived neuronal-like cell line PC-12 were purchased from ATCC.

Techniques: Control, Liposomes, Formulation

Journal: RSC Advances

Article Title: Comparative evaluation of donepezil-loaded polymeric and liposomal nanoparticles for Alzheimer's disease: biocompatibility, drug release kinetics, and cellular uptake study

doi: 10.1039/d6ra00929h

Figure Lengend Snippet: In vitro cellular uptake of Rhodamine labelled DPPC-based liposomes (red) and FITC-labelled PCL/PVA nanoparticles (green) by ECV-304 and PC-12 cells after 24 hours of incubation period. Co-localization of the red fluorescence (liposomes) or green fluorescence (PCL/PVA NPs) in proximity to the blue DAPI-stained nuclei confirms the association of nanoparticles with ECV-304 and PC-12 cells, demonstrating either internalization or surface binding. Fluorescence microscopy was performed at 50× magnification; scale bar = 25 µm (consistent across all images).

Article Snippet: The human endothelial-like cell line ECV-304 and the immortalized rat-derived neuronal-like cell line PC-12 were purchased from ATCC.

Techniques: In Vitro, Liposomes, Incubation, Fluorescence, Staining, Binding Assay, Microscopy

Journal: RSC Advances

Article Title: Comparative evaluation of donepezil-loaded polymeric and liposomal nanoparticles for Alzheimer's disease: biocompatibility, drug release kinetics, and cellular uptake study

doi: 10.1039/d6ra00929h

Figure Lengend Snippet: Quantitative analysis of cellular uptake of rhodamine-labelled DPPC-based liposomes and FITC-labelled PCL/PVA NPs along with their respective free dye controls by ECV-304 and PC-12 cell lines. Both formulations showed significantly higher uptake than their respective free dye controls. PCL/PVA nanoparticles exhibited significantly higher uptake than liposomes in ECV-304 cells. Results are expressed as mean ± SD. Statistical significance was determined using a one-way ANOVA followed by Tukey's test to compare liposomes and nanoparticles uptake against their respective controls and denoted as follows: P < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****).

Article Snippet: The human endothelial-like cell line ECV-304 and the immortalized rat-derived neuronal-like cell line PC-12 were purchased from ATCC.

Techniques: Liposomes

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: Native NPM1 and YAP1 proteins form complexes in prostate cancer cell models (A) The Venn diagram illustrates proteins associated with YAP1 in LNCaP cells treated with dihydrotestosterone (DHT, 10 nM) or enzalutamide (ENZ, 20 μM) under dextran-coated charcoal-stripped (DCC) serum conditions. Unique and shared proteins for each treatment are indicated. (B) A protein interaction network generated using the GeneMania web portal positions NPM1 within the YAP1 network. (C) Western blot analysis of NPM1 protein levels in AR-positive (LNCaP, C4-2, C4-2B, and 22Rv1) and AR-negative (PC3 and ARCaP) cell lines . β-actin served as a loading control. (D) Quantitative PCR analysis showing correlation between NPM1 transcript and protein levels across the same cell lines. (E) Co-immunofluorescence staining of NPM1 (green) and YAP1 (red) in LNCaP and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (F) Western blot showing NPM1 in YAP1 immune complexes in nuclear extracts from LNCaP, C4-2, C4-2B, and PC3 cells. IgG served as a negative control . (G) Reciprocal co-IP using an NPM1 antibody demonstrates YAP1 presence in NPM1 immune complexes exclusively in PC3 cells. β-actin was used as a loading control. (H) Representative confocal images showing PLA foci (red) indicating YAP1-NPM1 interactions in LNCaP, C4-2, and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (I) Enlarged images of boxed regions from panel H highlight nuclear localization of PLA foci. (J) Quantification of PLA foci per cell across the indicated cell lines. Statistical significance was determined using a two-tailed t test (∗ p < 0.01). Data are represented as mean ± SEM.

Article Snippet: LNCaP (Cat# CRL-1740), C4-2 (Cat# CRL-3314), C4-2B (Cat# CRL-3315), 22Rv1 (Cat# CRL-2505), and PC3 (Cat# CRL-1435) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Generated, Western Blot, Control, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Negative Control, Co-Immunoprecipitation Assay, Two Tailed Test

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: NPM1 influences YAP1 activity and the regulation of its target genes in cellular contexts (A–C) Quantitative PCR analysis of NPM1, YAP1, and MYC mRNA levels in LNCaP and PC3 cells after transient transfection with scrambled or NPM1-specific siRNA. (D and E) Western blot analysis showing YAP1 and MYC protein levels in LNCaP and PC3 cells with or without NPM1 knockdown. (F–G) Quantitative PCR analysis of YAP1 target gene expression in LNCaP and PC3 cells transfected with scramble control or NPM1-specific siRNA (∗ p < 0.001; ∗∗ p < 0.01). Data are represented as mean ± SEM. (I–K) Quantitative PCR analysis of YAP1 target genes (CCN1, CCN2, and ANKRD1) in LNCaP cells after transfection with scramble control or NPM1-specific siRNA, followed by overnight treatment with EtOH (vehicle) or DHT under 5% CSS-fed conditions . Statistical significance was assessed using a two-tailed t test (∗ p < 0.05; ∗∗ p < 0.01). Data are presented as mean ± SEM.

Article Snippet: LNCaP (Cat# CRL-1740), C4-2 (Cat# CRL-3314), C4-2B (Cat# CRL-3315), 22Rv1 (Cat# CRL-2505), and PC3 (Cat# CRL-1435) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Activity Assay, Real-time Polymerase Chain Reaction, Transfection, Western Blot, Knockdown, Targeted Gene Expression, Control, Two Tailed Test

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: Synergistic interactions between NPM1 and YAP1 regulate cell growth (A) Western blot analysis of NPM1 protein levels in LNCaP cells with or without NPM1 silencing by siRNA; β-actin served as a loading control. (B) Colony-forming ability of LNCaP cells with or without NPM1 knockdown, visualized by crystal violet staining. The accompanying graph presents quantification of colony numbers (∗ p < 0.01, two-tailed t test). (C and D) Dose-response curves for LNCaP, C4-2, C4-2B, and PC3 cells treated with NPM1 inhibitors NSC348884 or nucleozin. Graphs show log values of drug concentration versus percent cell growth; IC50 values were calculated for each cell line. (E–G) Cell-cycle distribution in LNCaP, C4-2, and PC3 cells treated with DMSO (mock), NSC348884, or nucleozin, as evaluated by flow cytometry. Graphs display the percentages of cells in the G1, S, and G2/M phases. (H) Confocal images showing YAP1–NPM1 interactions in LNCaP cells treated with DMSO, NSC348884, or nucleozin under serum-fed conditions. PLA was used to detect YAP1-NPM1 interactions (red foci); nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. The accompanying graph quantifies PLA foci. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are presented as mean ± SEM. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are represented as mean ± SEM.

Article Snippet: LNCaP (Cat# CRL-1740), C4-2 (Cat# CRL-3314), C4-2B (Cat# CRL-3315), 22Rv1 (Cat# CRL-2505), and PC3 (Cat# CRL-1435) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Western Blot, Control, Knockdown, Staining, Two Tailed Test, Concentration Assay, Flow Cytometry, CCK-8 Assay, Transfection

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: NPM1 regulates cell migration and shows increased interaction with YAP1 in high-grade prostate cancer tissues (A) Wound-healing assay images demonstrate a time-dependent delay in wound closure in LNCaP cells following NPM1 knockdown compared to scramble (Scram) siRNA control ( p < 1.14E−13). Scale bar: 10 μm. (B and C) Migration assays in LNCaP and PC3 cells show reduced motility upon NPM1 depletion in collagen-coated Boyden chambers, with or without EGF stimulation (∗ p < 0.01). Scale bar: 10 μm. Data are from two independent experiments performed in duplicate. (D) Representative PLA micrographs reveal increased YAP1-NPM1 interaction in high-grade tumors (GS > 7) versus low-grade (GS < 7) prostate cancer tissues ( n = 8). Scale bars: 10 and 5 μm, respectively. (E) Quantification of PLA foci in red (corresponding to D) ( n = 8). Data are expressed as mean ± SEM. (F) Schematic summary of findings created using BioRender.

Article Snippet: LNCaP (Cat# CRL-1740), C4-2 (Cat# CRL-3314), C4-2B (Cat# CRL-3315), 22Rv1 (Cat# CRL-2505), and PC3 (Cat# CRL-1435) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Migration, Wound Healing Assay, Knockdown, Control

Journal: bioRxiv

Article Title: Salvianolic acids are natural senolytics and increase lifespan in old age

doi: 10.64898/2026.04.29.721790

Figure Lengend Snippet: ( a ) A schematic workflow illustrating the preclinical therapeutic procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 recombinants, severe combined immunodeficient (M-NSG) mice were subject to either single agent or combinatorial treatment in a metronomic schedule of several cycles. The illustration was created in BioRender. ( b ) Comparative statistics of tumor end volumes. PC3 cancer cells were inoculated either alone or combined with PSC27 stromal cells before being implanted subcutaneously to the hind flank of M-NSG animals, which were administered with MIT and SAA, either alone or in combination. ( c ) Representative images of in vivo senescence in tumor foci by SA-β-gal staining. Scale bar, 50 μm. ( d ) Comparative statistics of tumor senescence as described in ( c ). ( e ) Transcriptional analysis of a subset of SASP factors expressed in epithelial vs. stromal cells acquired from tumor foci after laser capture microdissection (LCM) to isolate stromal and cancer cells, respectively. Signals were normalized to that of the sample with lowest value in the placebo group. ( f ) Transcriptional analysis of SASP factors and two canonical senescence biomarkers p16 INK4a and p21 CIP1 . ( g ) Statistical assessment of DDR and cellular apoptosis in tumors. Values are shown as the percentage of cells positively stained by IF or IHC specific to γH2AX or cleaved caspase 3 (CCL3), respectively. ( h ) Representative images of IHC staining for CCL3 at the completion of treatment regimens. Scale bar, 50 μm. ( i ) Comparative survival of animals sacrificed upon development of advanced bulky disease. Survival duration was calculated from tissue recombinant injection until death. P values were calculated by a two-sided log-rank (Mantel-Cox) test. DDR, DNA damage response. IF, immunofluorescence. IHC, immunohistochemistry. Data in b , d , e , f and g are shown as mean ± SD and representative of 3 independent biological replicates, with P values calculated by Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Article Snippet: The human prostate epithelial cancer cell line, PC3, was from ATCC and cultured with F-12K media (10% FBS).

Techniques: In Vivo, Staining, Laser Capture Microdissection, Immunohistochemistry, Recombinant, Injection, Immunofluorescence