Journal: Cancer Cell International

Article Title: Capsaicin combined with cisplatin inhibits TGF-β1-induced EMT and TSCC cells migration via the Claudin-1/PI3K/AKT/mTOR signaling pathway

doi: 10.1186/s12935-024-03485-0

Figure Lengend Snippet: CAP combined with DDP inhibits TGF-β1-induced EMT and TSCC cells migration through the Claudin-1/PI3K/AKT/mTOR signaling pathway. ( A ) The efficiency of AMPK knockdown is assessed by Western blot in HN6 cells ( B ) The levels of the EMT-related proteins p-AMPK and AMPK are detected by Western blot post 24 h of treatment with CAP and/or DDP in HN6 cells upon AMPK knockdown. * p < 0.05, ** p < 0.01 vs. T (shCon) group, # p < 0.05, ## p < 0.01 vs. T (shAMPK) group, & p < 0.05, && p < 0.01, T + C + D (shAMPK) group vs. T + C + D (shCon) group. ( C ) The efficiency of Claudin-1 (CLDN1) knockdown is assessed by Western blot in HN6 cells ( D ) The migration of cells is assessed by wound healing and Transwell assays. The migration of HN6 cells is induced by TGF-β1, and the closure distance and the number of migrated cells are photographed (×20) and measured post CAP and/or DDP treatment for 24 h. * p < 0.05, ** p < 0.01 vs. T (shCon) group, # p < 0.05, ## p < 0.01 vs. T (shCLDN1) group, & p < 0.05, && p < 0.01, T + C + D (shCLDN1) group vs. T + C + D (shCon) group ( E ) The PI3K/AKT signaling pathway is enriched by KEGG bioanalysis using the GOBP database ( F ) The levels of EMT-related proteins and the PI3K/AKT/mTOR signaling pathway are detected by Western blot post 24 h of treatment with CAP and DDP. * p < 0.05, ** p < 0.01 vs. the T(shCon) group; # p < 0.05, ## p < 0.01 vs. the T (shCLDN1) group; & p < 0.05, && p < 0.01, the T + C + D (shCLDN1) group vs. the T + C + D (shCon) group. T: TGF-β1, C: CAP, D: DDP. All data are presented as the mean ± SD of three independent experiments

Article Snippet: Anti-p-PI3K (AP0854, 1:1000) and anti-β-Actin (AC026, 1:8000) were purchased from ABclonal.

Techniques: Migration, Knockdown, Western Blot

Journal: Cancer Cell International

Article Title: Capsaicin combined with cisplatin inhibits TGF-β1-induced EMT and TSCC cells migration via the Claudin-1/PI3K/AKT/mTOR signaling pathway

doi: 10.1186/s12935-024-03485-0

Figure Lengend Snippet: Diagram of our conclusions in this article. CAP combined with DDP activated Claudin-1 to inhibit PI3K/AKT/mTOR phosphorylation and block TGF-β1-induced EMT and migration, while activating AMPK to reduce p-mTOR expression and inhibit non-TGF-β1-induced EMT and migration.

Article Snippet: Anti-p-PI3K (AP0854, 1:1000) and anti-β-Actin (AC026, 1:8000) were purchased from ABclonal.

Techniques: Blocking Assay, Migration, Expressing

Journal: Immunity, Inflammation and Disease

Article Title: Galectin‐9 alleviates acute graft‐versus‐host disease after haplo‐hematopoietic stem cell transplantation by regulating regulatory T cell/effector T cell imbalance

doi: 10.1002/iid3.1177

Figure Lengend Snippet: Gene expression profiles, functional analysis, and expression analysis of key proteins in PI3K/AKT/mTOR pathway in CD4 + T cell subsets. (A) Volcano plot of differentially expressed genes between patients with or without aGVHD. (B) GO analysis of differentially expressed genes. (C) KEGG analysis of differentially expressed genes. (D) Gene Set Enrichment Analysis (GSEA) was used to analyze the signaling pathways (PI3K/AKT/mTOR signaling pathway) enrichment in different groups. (E) PI3K/AKT/mTOR pathway protein expression in the peripheral blood was measured by western blot. Compared with the control group, * p < .05, ** p < .01; Compared with aGVHD(+) group, & p < .05, && p < .01. (F) Correlation analysis in patients without aGVHD. Data were analyzed with Spearman correlation analysis. (G) Galectin‐9 downregulates p‐PI3K in the Tim‐3 + CD4 + T cells in vitro. Tim‐3 + CD4 + T cells from patients with aGVHD were treated with or without rhGalectin‐9 for 48 h. The levels of p‐PI3K were determined by western blot. Compared with the PBS group, * p < .05, ** p < .01. Compared with the Galectin‐9 + IgG group, △ p < .05, △△ p < .01; Compared with Galectin‐9 + RAPA group, & p < .05, & & p < .01. (H) Analysis of IFN‐γ, IL‐4, IL‐17, and TGF‐β secretion by Tim‐3 + CD4 + T cells in vitro. Levels of IFN‐γ, IL‐4, IL‐17, and TGF‐β in culture supernatant were detected by ELISA. Compared with the PBS group, * p < .05, ** p < .01. Compared with the Galectin‐9 + IgG group, △ p < .05, △△ p < .01; Compared with the Galectin‐9 + RAPA group, & p < .05, & & p < .01. aGVHD, acute graft‐versus‐host disease; CBA, cytometric bead array; ELISA, enzyme‐linked immunosorbent assay; GO, Gene Ontology; IFN‐γ, interferon‐gamma; IL, interleukin; KEGG, Kyoto Encyclopedia of Genes and Genomes; PBS, phosphate‐buffered saline; TGF‐transforming growth factor.

Article Snippet: ABclonal Technology provided the PI3K p85α (cat#: A11526), Phospho‐PI3K P85α (Y467/Y199/Y464) (cat#: AP0854), and Phospho‐mTOR‐S2448 (cat#: AP0115) primary antibodies.

Techniques: Expressing, Functional Assay, Western Blot, In Vitro, Enzyme-linked Immunosorbent Assay, Saline

Journal: Immunity, Inflammation and Disease

Article Title: Galectin‐9 alleviates acute graft‐versus‐host disease after haplo‐hematopoietic stem cell transplantation by regulating regulatory T cell/effector T cell imbalance

doi: 10.1002/iid3.1177

Figure Lengend Snippet: Schematic diagram illustrating the hypothesis of signaling regulation in aGVHD. In patients with aGVHD, the expression of Tim‐3 is significantly increased. Galectin‐9 binding to Tim‐3 may inhibit the activation of the PI3K/AKT pathway and enhance the function of Treg cells. On the other hand, TGF‐β promotes the differentiation of Treg cells through autocrine secretion, while TGF‐β induces the expression of Galectin‐9 in a paracrine manner. The increased Treg cells can inhibit the activation of Th1 and Th17 cells by secreting TGF‐β, thus alleviating aGVHD by inducing immune tolerance. aGVHD, acute graft‐versus‐host disease; IFN‐γ, interferon‐gamma; IL, interleukin; TGF‐transforming growth factor.

Article Snippet: ABclonal Technology provided the PI3K p85α (cat#: A11526), Phospho‐PI3K P85α (Y467/Y199/Y464) (cat#: AP0854), and Phospho‐mTOR‐S2448 (cat#: AP0115) primary antibodies.

Techniques: Expressing, Binding Assay, Activation Assay