Journal: bioRxiv

Article Title: Multi-omic profiling of human antibody-secreting cells reveals diverse subsets sustain durable humoral immunity

doi: 10.64898/2026.04.13.717827

Figure Lengend Snippet: A) Experimental diagram. B) wnnUMAPs of ASCs colored by tissue (left) or subset (right). Data from HD matched fixed CITEseq. C) Percent subset of total ASCs by sample. Data from HD matched fixed CITEseq. D) Percent subisotype usage by sample. Data from HD matched fixed CITEseq. E) Experimental diagram. F) Representative region of interest from a bone marrow core colored by fluorescence signal (top) or subset labels of segmented cells (bottom). Data from HD BM spatial proteomics. G) Percent ASC subset of total cells by individual. Data from HD BM spatial proteomics. H) Computational diagram. I) Observed (black diamond) and randomly permuted (grey density) percent of ASCs found in homotypic niches (defined as all ASCs in a niche having identical subset identities), by individual. Empirical p-values calculated as the number of permutations with homotypic niche frequencies greater or equal to the observed homotypic niche frequency, divided by the number of permutations plus one. Data from HD BM spatial proteomics. J) Computational diagram. K) Scaled enrichment scores of cell types (x-axis) in ASC subset (y-axis) niches by individual (panel). Q-values<0.1 were colored white. Data from HD BM spatial proteomics. L) Representative images (panels) of ASC-rich regions colored by fluorescence signal (left) or cell type labels of segmented cells (right). Data from HD BM spatial proteomics.

Article Snippet: For the ASC culture condition screen, total BM ASCs were stimulated for 72 hours with CpG ODN 2006 (10μg/mL, Invivogen) or BCR crosslinker (anti-kappa light chain; 1μg/mL, Southern Biotech) with various combinations of stimulatory reagents, including MEGACD40L (0.1μg/ml, Enzo Life Sciences), BAFF (1μg/mL, PeproTech), CXCL12 (0.1μg/ml, R&D Systems), IL-2 (0.1μg/mL, Biolegend), and IL-21 (0.1μg/mL, PeproTech).

Techniques: Fluorescence, Spatial Proteomics

Journal: bioRxiv

Article Title: Multi-omic profiling of human antibody-secreting cells reveals diverse subsets sustain durable humoral immunity

doi: 10.64898/2026.04.13.717827

Figure Lengend Snippet: A) Experimental diagram. B) Serum Ig concentrations of patients with NDMM by timepoint (x-axis), isotype (y-axis), and the isotype of each patient’s malignant cell (shapes). Transparency indicates values outside the healthy reference ranges specified in the clinical reports. Data from clinical quantitative Ig assay. C) Percent ASCs of total BMMCs for HDs (left) and patients with NDMM, by timepoint (x-axis). Crossbar indicates mean. Q-values calculated by Wilcoxon rank sum test with FDR correction, comparing to HDs. Data from MM longitudinal BM CITEseq. *Q<0.1; **Q<0.01; ***Q<0.001 D) Percent non-malignant ASCs of total ASCs for patients with NDMM, by timepoint (x-axis). Crossbar indicates mean. Q-values calculated by Wilcoxon rank sum test with FDR correction, comparing to PRETX. Data from MM longitudinal BM CITEseq. ***Q<0.001 E) Percent non-malignant ASC subset of total BMMCs for HDs (left) and patients with NDMM, by timepoint (x-axis) and subset (panels). Crossbar indicates mean. Q-values calculated by Wilcoxon rank sum test with FDR correction, comparing to HDs. Data from MM longitudinal BM CITEseq. *Q<0.1; **Q<0.01; ***Q<0.001

Article Snippet: For the ASC culture condition screen, total BM ASCs were stimulated for 72 hours with CpG ODN 2006 (10μg/mL, Invivogen) or BCR crosslinker (anti-kappa light chain; 1μg/mL, Southern Biotech) with various combinations of stimulatory reagents, including MEGACD40L (0.1μg/ml, Enzo Life Sciences), BAFF (1μg/mL, PeproTech), CXCL12 (0.1μg/ml, R&D Systems), IL-2 (0.1μg/mL, Biolegend), and IL-21 (0.1μg/mL, PeproTech).

Techniques:

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 ameliorates pathological symptoms in AOM/DSS-induced CRC mice. C, control group; M, model group; BH, high-dose Plantaricin BM-1 group; BL, low-dose Plantaricin BM-1 group; F, 5-fluorouracil group. (A) Modeling methods and treatment protocols for AOM/DSS-induced CRC in mice. (B) Representative photographs of colorectal length in AOM/DSS-induced CRC mice and normal mice. (C) Colorectal length of each group of colitis-associated CRC mice after treatment with different reagents. (D) Changes in body weight of mice. (E) The number of tumors in each group of colitis-associated CRC mice was treated with different reagents. n = 8. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Control

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 ameliorates AOM/DSS-induced inflammation and histopathological features in CRC mice. C: control group; M: model group; BH: high-dose Plantaricin BM-1 group; BL: low-dose Plantaricin BM-1 group; F: 5-fluorouracil group. (A) Concentration of IL-1β in mouse serum, measured using an ELISA kit. (B) Serum concentrations of TNF-α in mice. (C) H&E-stained colorectal pathological sections of normal, AOM/DSS model, Plantaricin BM-1 and 5-FU groups. n = 8. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Control, Concentration Assay, Enzyme-linked Immunosorbent Assay, Staining

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 enhances T-cell numbers at the single-cell level. (A) Cell distribution in the AOM/DSS model group was visualized by UMAP and colored by cluster number in scRNA-seq. (B) Cell distribution in the high-dose Plantaricin BM-1 group, visualized by UMAP and colored by cluster number in scRNA-seq. (C) Cell distribution in the AOM/DSS model group, visualized by UMAP and colored by major cell type compartments in scRNA-seq. (D) Cell distribution in the high-dose Plantaricin BM-1 group was visualized by UMAP and colored with major cell-type compartments in scRNA-seq. (E) Histogram showing cell type variation across groups. (F) Bubble plots showing the expression of cell type markers. n = 3.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Single Cell, Expressing

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 increases the number of CD8 + T cells at the single-cell level. M: model group; BH: high-dose Plantaricin BM-1 group; BL: low-dose Plantaricin BM-1 group. (A) T cell distribution in the AOM/DSS model group, visualized by UMAP and colored by cluster number in scRNA-seq. (B) T cell distribution in the high-dose Plantaricin BM-1 group, visualized by UMAP and colored by cluster number in scRNA-seq. (C) Distribution of T cell subpopulations in the AOM/DSS model group, visualized by UMAP and colored by major cell type compartments in scRNA-seq. (D) Distribution of T cell subpopulations in the high-dose Plantaricin BM-1 group, visualized by UMAP, and colored by major cell type compartments in scRNA-seq. (E) Histogram showing changes in T cell subpopulation across groups. (F) Bubble plots showing the expression of T cell subpopulation markers. n = 3. (G) Immunofluorescence staining showed the expression of CD8, a CD8 + T-cell marker, in the colonic tissues of the model group, the high-dose Plantaricin BM-1 group, and the low-dose Plantaricin BM-1 group (n = 8). *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Single Cell, Expressing, Immunofluorescence, Staining, Marker

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 targets CD8 + T cells via the MAPK pathway within the T cell receptor signaling pathway. (A) Volcano plot of DEGs between scRNA-seq samples with or without Plantaricin BM-1 treatment, with red and blue dots indicating significantly up-and down-regulated genes, respectively (B) GO enrichment analysis results of DEGs. (C) KEGG enrichment analysis results of DEGs. KEGG enrichment analysis results of DEGs in T cells (D) , regulatory CD8 + T cells (E) , and CD8 + T cells (F) . (G) Venn diagram showing overlapping genes among the T cell receptor signaling pathway, MAPK signaling pathway, and DEGs in CD8 + T cells. (H) GSEA analysis results of the T cell receptor signaling pathway and MAPK signaling pathway in DEGs of CD8 + T cells. n = 3.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques:

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Plantaricin BM-1 inhibits CD8 + T apoptosis through the ERK/AP1/Bim pathway and enhances CD8 + T anti-cancer activity. (A) Volcano plot of DEGs in CD8 + T cells between scRNA-seq samples with and without Plantaricin BM-1 treatment. Red and blue dots represent significantly up-and down-regulated genes, respectively. (B) Violin plots showing differential expression of Ptpn6 , Bcl2l11 , Fos , Jun , Mapk1 , and Raf1 genes in CD8 + T cells between scRNA-seq samples with or without Plantaricin BM-1 treatment. (C) t-SNE plot showing expression of Ptpn6 , Bcl2l11 , Fos , Jun , Mapk1 , and Raf1 genes in CD8 + T cells. (D) Violin plots showing differential expression of Gzmb , Gzma , Fasl , Tox , and Cxcr6 genes in CD8 + T cells between scRNA-seq samples with or without Plantaricin BM-1 treatment. (E) t-SNE plot showing the expression of Gzmb , Gzma , Fasl , Tox , and Cxcr6 genes in CD8 + T cells. n = 3.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Activity Assay, Quantitative Proteomics, Expressing

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: ERK/AP1/Bim pathway scoring and analysis. C: control group; M: model group; BH: high-dose Plantaricin BM-1 group; BL: low-dose Plantaricin BM-1 group. (A) Box line plots showing ERK/AP1/Bim pathway scores of CD8 + T cells in the AOM/DSS model group and the Plantaricin BM-1 treatment group (n = 3). (B) UMAP plots of ERK/AP1/Bim pathway scores, with each cell’s scores represented by varying shades. RT-qPCR analysis of Fos (C) , Bcl2l11 (D) , Mapk1 (E) , and Jun (F) mRNA expression in mouse CRC tissues. (G) Immunohistochemical analysis of ERK protein expression in colonic tissues. n = 8. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Control, Quantitative RT-PCR, Expressing, Immunohistochemical staining

Journal: Frontiers in Immunology

Article Title: Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK/AP1/Bim signaling pathway

doi: 10.3389/fimmu.2026.1792962

Figure Lengend Snippet: Flow cytometry analysis of CD8 + T cells and Western blot analysis of pathway proteins. C: control; BH: high-dose Plantaricin BM-1 (10,240 AU/ml); BL: low-dose Plantaricin BM-1 (5,120 AU/ml); Inhibitor: intervention with ERK inhibitor. (A) Flow cytometry detection of apoptosis of mouse spleen CD8 + T cells after 72h of the action of different concentrations of Plantaricin BM-1 (blank control, 2560 AU/ml, 5120 AU/ml, 7680 AU/ml, and 10240 AU/ml). (B) Western blot analysis of the expression of ERK/AP1/Bim pathway-related proteins (including ERK and Bim) as well as β-actin in the splenic CD8 + T cells of mice after treatment with Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml) and inhibitors (n = 8). *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

Article Snippet: To assess the effects of Plantaricin BM-1 on ERK and Bim, we treated complete culture medium (negative control), different concentrations of Plantaricin BM-1 (5120 AU/ml and 10240 AU/ml), along with the ERK inhibitor SCH772984 (MCE, Shanghai, China, 0.5 μM, positive control) to treat mouse spleen CD8 + T cells, followed by incubation for 1 hour.

Techniques: Flow Cytometry, Western Blot, Control, Expressing

Journal: Scientific Reports

Article Title: VS-4718 enhances apoptosis induced by low-dose carfilzomib and overcomes carfilzomib resistance in PSMB5 -mutated proteasome inhibitor resistant multiple myeloma

doi: 10.1038/s41598-026-43205-4

Figure Lengend Snippet: Impact of VS-4718 alone and in combination with carf on survival in seven MM cell lines. ( A – H ) MM cells were treated with 1 µM VS and moderate concentrations of carf alone and in combination. Suitable concentrations of carf were determined individually for each MM cell line. Survival was determined by Annexin V-647/PI staining and subsequent FACS analysis. ( A ) An experiment with the AMO-1 cell line was used to illustrate the gating strategy employed here and in further FACS experiments. ( B – H ) For the graphical representation, the annexin V/PI negative fraction was calculated relative to that in the DMSO-treated control sample (% annexin V/PI neg. cells rel. ctrl.). Bars represent mean ± SD of ≥ three independent experiments, except for KMS-12-BM (2 rounds). P -values were determined in an ordinary one-way ANOVA using Tukey’s multiple comparison test and depicted only for p < 0.05. Only statistical comparisons between DMSO control and treated cells as well as single drugs vs. drug combinations were depicted to focus on the relevant comparisons.

Article Snippet: The parental human multiple myeloma cells (pHMCLs) (L-363, AMO-1, U-266, KMS-12-BM, JJN.3 (DSMZ, Braunschweig, Germany) KMS-11 (Japanese Collection of Research Bioresources (JCRB)), MM1.S (LGC Biolabs, Wesel, Germany)) which were derived from MM patients at different clinical stages and represent different molecular profiles , were cultured in RPMI-1640 medium supplemented with 10% FBS, 2 mM L-glutamine and 1 mM sodium pyruvate .

Techniques: Staining, Control, Comparison

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: Synthesis, morphology, and structural characterization of FBR-NDs. a the Structure of BMS-1, and R848. b the solution of Fe³⁺, BMS-1, and R848 to synthesize FBR nanoparticles using the nanoprecipitation method. c TEM images of FBR-NDs (top) and the binary control FB-NDs (Fe 3+ /BMS-1 without R848, bottom, scale bar = 50 nm. The comparison confirms that R848 encapsulation does not alter the spherical morphology. d DLS analysis of FBR-NDs showing particle size distribution (50.43 ± 21.8 nm) and PDI = 0.207. e TEM mapping and EDX spectrum showing elemental distribution (C, Fe, O, N) in FBR-NDs. f XPS survey and high-resolution spectra of FBR-NDs (Fe 2p, N 1s, O 1s). g Deconvolution of O 1s and Fe 2p XPS peaks for FBR-NDs. h XRD pattern of FBR-NDs, indicating amorphous structure. i FT-IR spectra of BMS-1, R848, FeCl₃, and FBR-NDs showing functional group incorporation

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Control, Comparison, Encapsulation, Functional Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: Drug loading, release, and redox-responsive properties. a UV-Vis spectra of FeCl₃, BMS-1, R848, and FBR-NDs. b pH-responsive drug release profiles of BMS-1 and R848 from FBR-NDs. c GSH-responsive drug release (top) and absorbance profiles of BMS-1-loaded FBR-NDs (bottom). d Fe²⁺ release profile in response to GSH concentration (ICP-OES determined Fe content: 18.2 wt%). e CDT analysis of FBR-NDs under 10 mM GSH, showing color change and absorbance decline. f Stability analysis of FBR-NDs in PBS and 10% FBS over 10 days. g Dissociation of FBR-NDs under EDTA, Tween 80, urea, and NaCl conditions after 24 h

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Concentration Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs Inhibit Breast Cancer Cell Growth in vitro. a Cell viability of BT549 and MDA-MB-231 cells treated with PBS, R848, BMS-1, R848 + BMS-1, Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs for 48 h, determined using MTT assays. Cell viability was significantly reduced in the Fe 3+ -containing groups, with the most pronounced cytotoxicity observed in FBR-NDs-treated cells. b Colony formation assay in BT549 and MDA-MB-231 cells following treatment. The number of colonies was significantly reduced in Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs-treated cells. c DNA replication capacity in treated BT549 and MDA-MB-231 cells. The ability to replicate DNA was significantly diminished in Fe 3+ -containing groups, especially in the FBR-NDs-treated group. d Caspase-3/7 activity was measured in BT549 and MDA-MB-231 cells. Treatment with Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs led to a significant increase in caspase-3/7 activity, indicating enhanced apoptosis. e Senescence-associated β-galactosidase (SA-β-gal) staining in treated cells. FBR-NDs treatment resulted in a significant increase in senescence. f TUNEL staining in BT549 and MDA-MB-231 cells. The number of TUNEL-positive cells increased significantly in Fe 3+ -R848, Fe 3+ -BMS-1, and FBR-NDs-treated cells, with FBR-NDs showing the most prominent effect

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: In Vitro, Colony Assay, Activity Assay, Staining, TUNEL Assay

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs Induce Ferroptosis in Breast Cancer Cells. a , b , Measurement of GSH/GSSG A, and NADP+/NADPH B, ratios in BT549 and MDA-MB-231 cells following treatment with Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs. Both ratios were significantly reduced after treatment, with the most significant decrease observed in the FBR-NDs-treated group. c , d , ROS C, and lipid peroxidation D, levels in BT549 and MDA-MB-231 cells treated with Fe 3+ -R848, Fe 3+ -BMS-1, or FBR-NDs. Both ROS and lipid peroxidation levels were significantly elevated, particularly in FBR-NDs-treated cells. e TEM analysis of mitochondrial morphology in BT549 and MDA-MB-231 cells after treatment. Mitochondria exhibited swelling, blurred inner membrane structure, increased membrane folding, and ruptured outer membranes. Vesicular structures were also observed in the membrane and endoplasmic reticulum, indicative of ferroptosis. f Expression levels of ferroptosis-related markers GPX4, TLR4, ACXL4, and FSP1 in treated BT549 and MDA-MB-231 cells. FBR-NDs treatment significantly decreased GPX4 and FSP1 expression while increasing TLR4 and ACXL4 expression, suggesting the promotion of ferroptosis

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: Membrane, Expressing

Journal: Breast Cancer Research : BCR

Article Title: FBR-NDs: a ferroptosis-inducing nanocomplex for targeted breast cancer therapy via immune modulation and redox-responsive drug delivery

doi: 10.1186/s13058-026-02247-2

Figure Lengend Snippet: FBR-NDs inhibit tumor growth in vivo. a schematic illustration of the treatment schedule. Treatments were administered via tail vein injection at a dose equivalent to 5 mg/kg Fe every 3 days starting when tumor volumes reached ~ 100 mm³. b Tumor volume, c tumor weight, and growth curves d , in C57BL/6 mice bearing 4T1 tumors. FBR-NDs treatment resulted in a significantly lower tumor growth rate compared to PBS, R848, BMS-1, and R848 + BMS-1 treatments. Fe 3+ -R848 and Fe 3+ -BMS-1 also showed reduced tumor growth, but FBR-NDs were the most effective. e - f , Immunohistochemical staining of Ki67 ( e ), and Cleaved-Caspase-3 ( f ), in tumor tissues. FBR-NDs-treated tumors showed significantly reduced Ki67-positive cells and increased Cleaved-Caspase-3 positivity, indicating inhibited proliferation and enhanced apoptosis. g 4-HNE staining of tumor tissues to detect lipid peroxidation. The strongest 4-HNE staining was observed in tumors treated with FBR-NDs, indicating the highest induction of ferroptosis. h , i Immunohistochemical staining for GPX4 ( h ), and TLR4 ( i ), in tumor tissues. Treatment with FBR-NDs significantly reduced GPX4 expression and increased TLR4 expression, confirming ferroptosis induction. j Kaplan-Meier survival curves of 4T1 tumor-bearing mice in different treatment groups. Statistical significance was calculated using the Log-rank (Mantel-Cox) test

Article Snippet: In this process, Fe3+ (from FeCl3), BMS-1 [PD-1/PD-L1 inhibitor, purity 98%, Cat. No. HY-19991, MedChemExpress (MCE)], and R848 (Resiquimod, purity 98%, Cat. No. HY-13740, MCE) were mixed in appropriate molar ratios.

Techniques: In Vivo, Injection, Immunohistochemical staining, Staining, Expressing