Journal: bioRxiv

Article Title: Fitness and immune-escape within germinal centers shape premalignant evolution toward lymphoma

doi: 10.64898/2026.06.25.734549

Figure Lengend Snippet: (A) Experimental design for single-cell RNA sequencing of PD-1⁺ CD8⁺ T-cells sorted from recipient mice 10 days after immunization. (B) UMAP projection of PD-1⁺ CD8⁺ T-cells colored by annotated subset identity. (C) Dot plot showing expression of selected marker genes across annotated CD8⁺ T-cell subsets. (D) Density plots showing the distribution of PD-1⁺CD8⁺ T-cells from Ctrl, BC, and BCK recipients across the UMAP. (E) UMAP projections showing expression of selected marker genes from (C). (F) Slingshot trajectory analysis of PD-1⁺ CD8⁺ T-cell differentiation, highlighting trajectory path1 from activated states toward stem-like, early effector and effector states. (G) Comparison of CD8⁺ T-cell subset distribution along path 1, which terminates in cytotoxic effector differentiation. Quantification shows mean cluster proportion from two biological replicates. (H) Gene set enrichment analysis of HALLMARK pathways comparing cluster 4 from BCK and BC conditions. (I-K) TGF-β receptor blockade following GC response derived from transferred BCK B-cells. (I) Experimental design for LY2109761 treatment. (J) Left, representative gating of granzymeB⁺ perforin⁺ effector cells among PD-1⁺ CD8⁺ T-cells. Right, quantification of PD-1⁺ CD8⁺ T-cells and granzymeB⁺ perforin⁺ effector CD8⁺ T-cells per 10⁶ splenocytes. (K) Left, representative gating of donor-derived reporter⁺ CD45.2⁺ B-cells. Right, quantification of donor-derived reporter⁺ CD45.2⁺ GC B-cells per 10⁶ splenocytes. (L) Endogenous CD45.1⁺ GC B-cell response to SRBCs in the absence or presence of TGF-β receptor inhibition with LY2109761. Left representative gating of host CD45.1⁺ GC B-cell B-cells. Right, quantification of host CD45.1⁺ GC B-cell B-cells. (M) Requirement for CD8⁺ T-cells during TGF-β receptor blockade. Top, schematic of experimental design. Bottom, representative gating of donor-derived reporter⁺ CD45.2⁺ B-cells from BCK recipients treated with LY2109761 together with isotype control or anti-CD8 antibody; and quantification of reporter⁺ CD45.2⁺ GC B-cells per 10⁶ splenocytes. Each symbol in (J, L, K, M) represents an individual mouse. Each symbol in (G) represents mean value from two biological replicates. (J-L) placebo n = 3, LY2109761 n = 3. (M) LY2109761 + isotype n = 3, LY2109761 + anti-CD8 n = 3. Small horizontal lines indicate mean ± SD. Data in (J-L) are representative of two independent experiments; data in (K) are representative of two independent experiments. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001; Two-way ANOVA in (G) , value calculated on two biological replicates from each group, remaining statistical calculations used unpaired two-tailed Student’s t test. ns, not significant.

Article Snippet: For TGF-β pathway inhibition, mice were treated with the dual TGF-β type I/II receptor inhibitor LY2109761 (MedChemExpress, HY-12075; 40 mg/kg).

Techniques: Single Cell, RNA Sequencing, Expressing, Marker, Cell Differentiation, Comparison, Derivative Assay, Inhibition, Control, Two Tailed Test

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes MMT in HPMCs through the TGF-β/Smad signaling pathway (A–D) WB analysis of TGF-β1 and p -Smad2/3 in HMrSV5 cells treated with CM from SGC-7901 cells (A and B) and HGC-27 cells (C and D) with different LGALS1 expression levels ( n = 3). (E–H) WB confirmed E-cadherin and vimentin expression in HMrSV5 cells treated with CM from SGC-7901 cells (E and F) and HGC-27 cells (G and H) with different LGALS1 expression levels or CM-OE- LGALS1 supplemented with ITD1. Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Techniques: Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Activation of the TGF-β/Smad signaling pathway promotes MMT in HPMCs (A–D) Representative immunofluorescence images of E-cadherin and vimentin in HMrSV5 cells treated with CM from SGC-7901 cells (A and B) and HGC-27 cells (C and D) with different LGALS1 expression levels or CM-OE- LGALS1 supplemented with ITD1 (Scale bars, 50 μm) ( n = 3). (E–H) Representative immunofluorescence images of TGF-β1 and p -Smad2/3 in HMrSV5 cells treated with CM from SGC-7901 cells (E and F) and HGC-27 cells (G and H) with different LGALS1 expression or CM-OE- LGALS1 supplemented with ITD1 (Scale bars, 50 μm) ( n = 3). Data are represented as mean ± SD.∗ p < 0.05, ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Techniques: Activation Assay, Immunofluorescence, Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: TGF-β/Smad signaling pathway is activated in peritoneal tissues undergoing MMT, and galectin-1 enhances GC cell adhesion to HPMCs via this pathway (A–C) Representative images of immunofluorescence for TGF-β1 (A) and p -Smad2/3 (B) in peritoneal tissues without or with MMT (×400 magnification). (C) Comparison of the relative fluorescence density of TGF-β1 and p -Smad2/3 in peritoneal tissues without or with MMT ( n = 6). (D and E) GC cells incubated with Calcein-AM were added to HMrSV5 cells treated with CM from SGC-7901 cells (D) or HGC-27 cells (E) or with different LGALS1 expression levels (Scale bars, 100 μm) ( n = 3). (F and G) Mean IODs of SGC-7901 cells (F) and HGC-27 cells (G) adherent to HMrSV5 cells ( n = 3). Data are represented as mean ± SD.∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Techniques: Immunofluorescence, Comparison, Fluorescence, Incubation, Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Galectin-1-induced peritoneal MMT through the TGF-β/Smad signaling pathway is an important mechanism for GCPM, offering a potential target for GC treatment.

Techniques: Animal Model, Staining, Immunofluorescence, Fluorescence