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

Journal: bioRxiv

Article Title: Fasting disrupts the InsP₆–HDAC3 axis to drive ER stress–mediated clearance of DNA-damaged cells and enforce tissue quality control

doi: 10.64898/2026.05.24.727426

Figure Lengend Snippet: (A) HDAC3 activity assay in GFD-treated HCT116 cells following stimulation (3 h) with TGFβ, IGF1, VEGF, EGF, FGF, or PDGF. (n = 3; mean ± SD). (B) Immunoblot analysis of H3K9ac, H3K27ac, H4K16ac, and HDAC3 in untreated, GFD, and growth factor-stimulated conditions. (n = 3). (C) Co-immunoprecipitation of HDAC3 from HCT116 cells overexpressing FLAG-SMRT deacetylase-activating domain (FLAG-DAD) under indicated conditions. (n = 3). (D) Immunoblot analysis of IPMK, CDK5RAP3, CHOP, IRE1, and H3K27ac following treatment with the TGFβ receptor inhibitor vactosertib in HCT116 cells. (n = 3). (E) HDAC3 enzymatic activity assay in HCT116 cells treated with TGF-β, and vactosertib. (n = 3; mean ± SD). (F) Immunoblot analysis of H3K27ac in untreated, GFD, vactosertib-treated, and HDAC3 knockout cells. (n = 3). (G) Immunoprecipitation of IPMK–myc followed by immunoblotting for FBXO22, SKP1, Cullin1, and K48-linked ubiquitin under the indicated conditions. (n = 3). (H) Co-immunoprecipitation of phosphorylated SMAD2/3 with FBXO22, SKP1, and Cullin1 under the indicated conditions. (n = 3). (I) Co-immunoprecipitation of phosphorylated SMAD2/3 with FBXO22–SCF–Cullin1 components following vactosertib treatment. (n = 3). (J) IPMK expression and pSMAD2/3 level after Verteportin (blocks pSmad2/3 nuclear localization) treatment. (n = 3). (K) Immunoprecipitation study to show effects of Verteportin on FBXO22 interaction with IPMK and pSMAD2/3. (n = 3).

Article Snippet: For the inhibition of TGF-β signaling, cells were treated with 1 μM Vactosertib (Cat. No. 19928 MCE chemicals) or 50 μM RepSoX (Cat no. HY-13012 MCE Chemical) overnight (approximately 16 hours) in complete growth media supplemented with serum.For the enteroid system, RepSOX treatment was administered for 6 hr at a dose of 50 μM.

Techniques: Activity Assay, Western Blot, Immunoprecipitation, Histone Deacetylase Assay, Enzyme Activity Assay, Knock-Out, Ubiquitin Proteomics, Expressing