Journal: Molecular Therapy Oncology

Article Title: Survivin/BIRC5-derived peptide disrupts survivin dimerization and cell division and induces multifaceted anti-cancer effects

doi: 10.1016/j.omton.2025.201123

Figure Lengend Snippet: Cell death induction by 1H13-survivin/BIRC5-derived peptides targeted to the cytoplasm, mitochondria, or nucleus (A) The sequences added to the 1H13-BIRC5 peptide to target it to the: (1) cytoplasm, (2) mitochondria, or (3) nucleus. The underlined sequence represents the 1H13 peptide; in red, amino acids indicate D-amino acid substitutions. (B) A549 cells were incubated for 90 min with 5 μM FITC-labeled, nucleus-targeted peptide IH13-Nuc, and were also IF-stained with anti--SMAC, anti-IP3R or anti-GM130 antibodies, and stained with DAPI to visualize the mitochondria, ER, Golgi, and nucleus, respectively. Confocal microscope images are shown, with white arrows indicating peptide co-localization with the mitochondria (SMAC). Orange and yellow arrows indicate peptide presence in the nucleus and cytosol, respectively. (C) A549 cells were incubated with the mitochondria- or nucleus-targeted 1H13-BIRC5-derived peptide for 24 h in serum-free medium, followed by a cell proliferation assay using the SRB method. (D and E) Apoptotic cell death as induced in A549 cells following incubation for 24 h with the nucleus-targeted peptide (2/3D-1H13-Nuc) in the presence or absence of the indicated concentrations of the peptides in serum-free medium and subjected to FITC–annexin V/PI staining, followed by a flow cytometry analysis. Representative histograms for control and selected peptide concentration (D) and analysis of early and late apoptotic stages are shown (E). (F and G) Cell death as induced by 2/3D-1H13-Nuc in different cell lines, A549, SH-SY5Y, U-87MG, PC-3, and HUV-EC-C (F) or Jurkat, K562, and KMH2-LC (G) were treated with the indicated concentrations of the peptide for 24 h, then subjected to cell death analysis using propidium iodide (PI) staining and flow cytometry. (H and I) A549 cells were seeded at a density of 2 × 10 5 cells per well in a 12-well plate. After 24 h, the cells were transfected with 2 μg of a pCMV3-survivin expression plasmid (HG10356-UT, Sino Biological, China) or with an empty pCMV3 plasmid (control) using JetPrime transfection reagent (Polyplus, France), following the manufacturer’s instructions. Twenty-four hours post-transfection, the cells were re-seeded at 1 × 10 5 cells per well in a 12-well plate. After another 24 h, the culture medium was replaced with serum-free medium, and the cells were treated with the indicated concentrations of the 2/3D-1H13-Nuc peptide. Survivin overexpression levels were assessed by immunoblotting (H), and cell death was analyzed by propidium iodide (PI) staining followed by FACS analysis (I). Results represent the means ± SEM ( n = 3).

Article Snippet: After 24 h, the cells were transfected with 2 μg of a pCMV3-survivin expression plasmid (HG10356-UT, Sino Biological, China) or with an empty pCMV3 plasmid (control) using JetPrime transfection reagent (Polyplus, France), following the manufacturer’s instructions.

Techniques: Derivative Assay, Sequencing, Incubation, Labeling, Staining, Microscopy, Proliferation Assay, Flow Cytometry, Control, Concentration Assay, Transfection, Expressing, Plasmid Preparation, Over Expression, Western Blot

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: A) Survival rate after 24 h FAC and 2 h DEM treatment. B, C) Labile Fe(II) levels measured as FerroOrange fluorescence after treatment with FAC and 2 h (B) or 24 h (C) treatment with DEM were normalized to worm autofluorescence and untreated control. D) Representative bright field, FerroOrange fluorescence (orange), and auto fluorescence (blue, excitation: 405 nm, emission: 455 nm) images of wild type worms after treatment with FerroOrange dye. E) Proteins encoded by DEGs of Fe-homeostasis after treatment for 2 h and 24 h with FAC, DEM, and FAC + DEM compared to untreated control. Shown are the mean ∓ SEM of ≥ 3 independent experiments. Significance is depicted as ∗ compared to untreated control. Transcriptomic analysis was performed from n = 3 independent experiments each. C. elegans /human orthologue: SMF-2/3/DMT-1: divalent metal transporter; FTN-1/-2/FTH and FTL: ferritin; F21D5.3/DCYTB: duodenal cytochrome B; FPN-1.1/1.2/FPN: ferroportin.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques: Fluorescence, Control

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: Relative gene expression after treatment with FAC or/and 2 h (A–F) or 24 h (G–L) treatment with DEM. Gene expression of A, G) smf-2 ; B, H) smf-3 ; C, I) ftn-1 ; D, J) ftn-2 ; E, K) fpn-1.1 and F, L) fpn-1.2 were determined via RT-qPCR. Shown are the mean + SEM of 3 independent experiments. Significance is depicted as ∗ compared to untreated control. C. elegans /human orthologue: SMF-2/3/DMT-1: divalent metal transporter; FTN-1/-2/FTH and FTL: ferritin; FPN-1.1/1.2/FPN: ferroportin.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques: Gene Expression, Quantitative RT-PCR, Control

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: Principal component analysis (PCA) of PC1 and PC3 after treatment with FAC and 2 h (A) or 24 h (B) with DEM. C) Proteins encoded by DEGs of GSH metabolism. Transcriptomic analysis was performed from n = 3 independent experiments each. C. elegans /human orthologue: GCS-1/GCLC: glutamate-cysteine ligase; E01A2.1/GCLM: glutamate-cysteine ligase catalytic subunit; GSS-1/GSS: glutathione synthase; GSR-1/GSR: glutathione disulfide reductase; GPX-1/2/GPX-4: glutathione peroxidase; GPX-3/5/GPX-3: glutathione peroxidase.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques:

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: A) Survival rate after 24 h FAC and 2 h DEM treatment. B, C) Labile Fe(II) levels measured as FerroOrange fluorescence after treatment with FAC and 2 h (B) or 24 h (C) treatment with DEM were normalized to worm autofluorescence and untreated control. D) Representative bright field, FerroOrange fluorescence (orange), and auto fluorescence (blue, excitation: 405 nm, emission: 455 nm) images of wild type worms after treatment with FerroOrange dye. E) Proteins encoded by DEGs of Fe-homeostasis after treatment for 2 h and 24 h with FAC, DEM, and FAC + DEM compared to untreated control. Shown are the mean ∓ SEM of ≥ 3 independent experiments. Significance is depicted as ∗ compared to untreated control. Transcriptomic analysis was performed from n = 3 independent experiments each. C. elegans /human orthologue: SMF-2/3/DMT-1: divalent metal transporter; FTN-1/-2/FTH and FTL: ferritin; F21D5.3/DCYTB: duodenal cytochrome B; FPN-1.1/1.2/FPN: ferroportin.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques: Fluorescence, Control

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: Relative gene expression after treatment with FAC or/and 2 h (A–F) or 24 h (G–L) treatment with DEM. Gene expression of A, G) smf-2 ; B, H) smf-3 ; C, I) ftn-1 ; D, J) ftn-2 ; E, K) fpn-1.1 and F, L) fpn-1.2 were determined via RT-qPCR. Shown are the mean + SEM of 3 independent experiments. Significance is depicted as ∗ compared to untreated control. C. elegans /human orthologue: SMF-2/3/DMT-1: divalent metal transporter; FTN-1/-2/FTH and FTL: ferritin; FPN-1.1/1.2/FPN: ferroportin.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques: Gene Expression, Quantitative RT-PCR, Control

Journal: Redox Biology

Article Title: Consequences of iron exposure and glutathione depletion on redox balance, lipidome, and neurotransmission in C. elegans

doi: 10.1016/j.redox.2026.104023

Figure Lengend Snippet: Proteins encoded by DEGs after short-term treatment with DEM and in combination with FAC of A) acetylcholine and B) serotonin-associated genes. Transcriptomic analysis was performed from n = 3 independent experiments each. C. elegans /human orthologue: UNC-13/UNC-13; ACE-2/BCHE: acetylcholinesterase; ACR-18/23: acetylcholine receptor; EAT-2/CHRNA-1: subunit of nicotinic acetylcholine receptor; TPH-1/TPH-1/2: tryptophan hydroxylase.

Article Snippet: Following Taqman probes were used: smf-2 (Ce02496629_g1), smf-3 (Ce02461545_g1), ftn-1 (Ce02477612_g1), ftn-2 (Ce02415799_g1), fpn-1.1 (Ce02414545_m1), fpn-1.2 (Ce02471200_g1) [ ].

Techniques:

Journal: bioRxiv

Article Title: Polymer-lipid hybrid nanoparticle enhances mRNA delivery and T cell-mediated immunity

doi: 10.64898/2026.01.22.701138

Figure Lengend Snippet: (a) Schematic illustration of the design of LNP and PLNP. (b) Left: sizes of LNP and PLNP measured by dynamic light scattering (DLS). Right: TEM images of LNP and PLNP. Scale bars: 100 nm. (c) Polydispersity index (PDI) of LNP and PLNP. (d) mRNA encapsulation efficiencies of LNP and PLNP. (e) Spike mRNA translation in RAW 264.7 macrophages after incubation with spike mRNA-loaded LNP or PLNP for 48 hours. Spike expression were measured by flow cytometry. Dose: 1 µg mRNA/mL. n = 3. (f) FLuc mRNA translation in RAW 264.7 macrophages on day 1, 2, 3, and 5 after incubation with FLuc mRNA-loaded LNP or PLNP. Dose: 1 µg mRNA/mL. n = 3. The FLuc signals were normalized to the day-1 signal of LNP-treated group. (g) Left: Representative flow plots of CD11c + DCs expressing SIINFEKL/H-2K b after incubation with OVA mRNA-loaded LNP or PLNP for 48 hours. Right: The percentages of CD11c + SIINFEKL/H-2K b+ DCs in total DCs. Dose: 1 µg mRNA/mL. n = 3. (h) Intracellular cytokine levels in RAW 264.7 macrophages after incubation with spike mRNA-loaded LNP, spike mRNA-loaded PLNP, empty LNP, or empty PLNP for 24 hours. Left: IFN-γ. Middle: TNF-α. Right: IL-2. Dose: 1 µg mRNA/mL. n = 3. (i) Cytokine secretion from human PBMCs after incubation with spike mRNA-loaded LNP, spike mRNA-loaded PLNP, empty LNP, or empty PLNP for 24 hours. Dose: 1 µg mRNA/mL. n = 3. (j) Schematic illustration of PLNP enhancing antigen presentation and proinflammatory cytokine generation in APCs. Data are presented as mean ± s.e.m. Statistical significance was determined using two-sided unpaired t-test (d, e, g), one-way ANOVA with Tukey post hoc test for multiple comparisons (h), or two-way ANOVA with Tukey post hoc test for multiple comparisons ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, and ****P < 0.0001.

Article Snippet: Wild-type SARS-CoV-2 spike encoding plasmid was obtained from the MacMaster lab. Omicron spike (B.1.1.529), influenza A H1N1 (A/Puerto Rico/8/1934) hemagglutinin (HA), and FLuc sequences were obtained from commercially available omicron spike, HA, and FLuc Gene ORF cDNA clone expression plasmids (Sino Biological #VG40835-UT, Sino Biological #VG11684-UT, and Addgene #101156) and inserted into the same plasmid backbone using Gibson assembly.

Techniques: Encapsulation, Incubation, Expressing, Flow Cytometry, Immunopeptidomics

Journal: bioRxiv

Article Title: Polymer-lipid hybrid nanoparticle enhances mRNA delivery and T cell-mediated immunity

doi: 10.64898/2026.01.22.701138

Figure Lengend Snippet: (a) Left: In vivo luminescence images of BALB/c mice treated with 1×PBS, FLuc mRNA-loaded LNP, or FLuc mRNA-loaded PLNP at 4, 24, 48, 72, and 96 hours post administration. Right: In vivo luminescence signals measured by integration of total flux for each mouse. Dose: 5 µg mRNA/mouse. N = 5. (b) Left: Fluorescence images of lymph nodes collected from C57BL/6 mice at 24 h post vaccination with DiD-labeled spike mRNA-loaded LNP or PLNP. Right: Quantification of LNP and PLNP accumulation in lymph nodes at 24 h post vaccination. Dose: 10 µg mRNA/mouse. n = 4. (c) Innate immune cell activation (CD86 + ) at 7 days post boost vaccination. C57BL/6 mice were vaccinated with spike mRNA-loaded LNP or PLNP on day 0 and boosted with same doses on day 21. Dose: 10 µg mRNA/mouse. n = 5. Left: DCs. Middle: Macrophages. Right: Monocytes. (d) Schematic illustration of PLNP enhancing lymph node targeting and innate immune cell activation. Data are presented as mean ± s.e.m. Statistical significance was determined using two-way ANOVA with Tukey post hoc test for multiple comparisons (a) or one-way ANOVA with Tukey post hoc test for multiple comparisons (b, c). ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, and ****P < 0.0001.

Article Snippet: Wild-type SARS-CoV-2 spike encoding plasmid was obtained from the MacMaster lab. Omicron spike (B.1.1.529), influenza A H1N1 (A/Puerto Rico/8/1934) hemagglutinin (HA), and FLuc sequences were obtained from commercially available omicron spike, HA, and FLuc Gene ORF cDNA clone expression plasmids (Sino Biological #VG40835-UT, Sino Biological #VG11684-UT, and Addgene #101156) and inserted into the same plasmid backbone using Gibson assembly.

Techniques: In Vivo, Fluorescence, Labeling, Activation Assay