pi 103  (Selleck Chemicals)

Journal: bioRxiv

Article Title: LncRNA YIYA enhances pancreatic cancer proliferation under high-glucose conditions through RAS–PKM2–mediated metabolic reprogramming that reinforces the Warburg phenotype

doi: 10.1101/2025.10.30.685546

Figure Lengend Snippet: (a) Kaplan–Meier survival plots showing the association of KRAS expression with overall survival in pancreatic cancer generated using the GEPIA2 database ( http://gepia2.cancer-pku.cn ). (b) Relative mRNA and (c) protein expression of KRAS in the MIA PaCa-2 cells cultured under NG or HG conditions. (d) Relative mRNA and (e) protein expression of KRAS in the spheroids of MIA PaCa-2 cells cultured under NG or HG conditions. (f) Immunofluorescence images representing KRAS expression and localization in MIA PaCa-2 cells grown under NG or HG conditions (Scale Bar: 20 µm). (g) Immunoblot images representing phospho AKT (pAKT) and total AKT (tAKT) expression in MIA PaCa-2 cells grown under NG or HG. (h) Relative lncRNA YIYA expression upon KRAS inhibition (KRASi; Adagrasib dose∼100 nM) in MIA PaCa-2 cells grown under HG conditions. (i) Relative lncRNA YIYA expression in HG cultured spheroids of MIA PaCa-2 cells upon KRAS inhibition (KRASi; Adagrasib dose∼100 nM) (The inhibitor was added to the medium mixture containing methylcellulose and HG media, and spheroids were subsequently allowed to form). (j) Relative lncRNA YIYA expression upon AKT inhibition (AKTi; PI103, dose∼1 μM) in MIA PaCa-2 cells grown under HG conditions. The glucose concentration used for NG is 5.5 mM, and for HG is 25 mM. Unless otherwise specified, treatments were carried out for 48 h. For quantitative comparisons, bar graphs representing gene expression or protein levels were normalized to the respective housekeeping gene or loading control (either GAPDH or β-actin). Fold change values shown in the graphs are expressed relative to the control, which was set to 1. All results are presented as mean ± SD from at least three independent experiments (n = 3). For comparisons involving multiple groups across varying concentrations and/or time points, two-way ANOVA followed by Tukey’s multiple comparisons post-test was performed. Statistical significance is indicated as (*) p < 0.05, (**) p<0.01, and (***) p < 0.001 versus the control. For pairwise comparisons between two groups, unpaired t-tests were applied.

Article Snippet: KRAS inhibitor (HY-130149), AKT inhibitor (HY-10115), Protein A/G magnetic beads (HY-K0202), and PKM2 inhibitor (HY-103617) were procured from MedChemExpress.

Techniques: Expressing, Generated, Cell Culture, Immunofluorescence, Western Blot, Inhibition, Concentration Assay, Gene Expression, Control

Journal: Materials Today Bio

Article Title: Rapamycin-induced small extracellular vesicles under GelMA scaffolds facilitate diabetic wound repair through accelerating angiogenesis and alleviating macrophage-mediated inflammation via PI3K/Akt signaling pathway

doi: 10.1016/j.mtbio.2025.101846

Figure Lengend Snippet: Alterations of transcriptome profile in diabetic wound tissue after being treated with RAPA-sEVs. ( A ) Volcano plot exhibited differentially expressed genes (DEGs) between hydrogel and hydrogel + sEVs2 groups. ( B ) Heatmap of transcriptomics clustering. ( C ) KEGG pathway analysis. ( D ) GO enrichment analysis. ( E ) Gene set enrichment analysis (GSEA) of PI3K/Akt signaling pathway. ( F ) The networks of protein–protein interaction (PPI). ( G-I ) The protein levels of p-PI3K, PI3K, p-AKT and AKT and the related quantitative analysis. Mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: PI-103 (S1038, Selleck, USA), a PI3K inhibitor, was utilized to investigate the role of the PI3K/Akt signaling pathway in RAPA-sEV-induced anti-inflammatory and pro-angiogenic effects.

Techniques:

Journal: Materials Today Bio

Article Title: Rapamycin-induced small extracellular vesicles under GelMA scaffolds facilitate diabetic wound repair through accelerating angiogenesis and alleviating macrophage-mediated inflammation via PI3K/Akt signaling pathway

doi: 10.1016/j.mtbio.2025.101846

Figure Lengend Snippet: Blockade of the PI3K/Akt pathway abrogates RAPA-sEV-mediated inhibition of macrophage proliferation and inflammatory factors. ( A-B ) Ki67 immunofluorescent staining of macrophages and the percentage of Ki67 positive cells (%) after being treated with PI3K inhibitor PI103. Scale bar, 100 μm. ( C ) The mRNA expression levels of inflammatory cytokines, including TNF-α, IL-1β, iNOS, in macrophages subjected to various treatments. Mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: PI-103 (S1038, Selleck, USA), a PI3K inhibitor, was utilized to investigate the role of the PI3K/Akt signaling pathway in RAPA-sEV-induced anti-inflammatory and pro-angiogenic effects.

Techniques: Inhibition, Staining, Expressing

Journal: Materials Today Bio

Article Title: Rapamycin-induced small extracellular vesicles under GelMA scaffolds facilitate diabetic wound repair through accelerating angiogenesis and alleviating macrophage-mediated inflammation via PI3K/Akt signaling pathway

doi: 10.1016/j.mtbio.2025.101846

Figure Lengend Snippet: Blocking the PI3K/Akt pathway attenuates the inhibitory effect of RAPA-sEVs on the migration of macrophages. ( A ) Scratch tests were utilized to evaluate macrophage migration with different treatments. Scale bar, 200 μm. ( B ) Transwell assays were employed to assess the migration ability of macrophage after treatment with PI103. Scale bar, 100 μm. ( C-D ) Quantification on the migrative area and number of macrophages with different therapeutic interventions. Mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: PI-103 (S1038, Selleck, USA), a PI3K inhibitor, was utilized to investigate the role of the PI3K/Akt signaling pathway in RAPA-sEV-induced anti-inflammatory and pro-angiogenic effects.

Techniques: Blocking Assay, Migration

Journal: Materials Today Bio

Article Title: Rapamycin-induced small extracellular vesicles under GelMA scaffolds facilitate diabetic wound repair through accelerating angiogenesis and alleviating macrophage-mediated inflammation via PI3K/Akt signaling pathway

doi: 10.1016/j.mtbio.2025.101846

Figure Lengend Snippet: Inhibition the PI3K/Akt pathway impairs the stimulative effect of RAPA-sEVs on the migration and tube formation abilities of HUVECs. ( A ) The migration capacity of HUVECs was detected by scratch tests after being treated with PI103. Scale bar, 200 μm. ( B ) Quantitative analysis of migrative area (mm 2 ). ( C ) Transwell assays were utilized to evaluate the migration of HUVECs. Scale bar, 100 μm. ( D ) Quantitative analysis of the number of migrated cells. ( E ) Tube formation assays were applied to assess the angiogenesis with different treatments. Scale bar, 400 μm. ( F-H ) Quantification of the number of nodes, junctions and branches. Mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: PI-103 (S1038, Selleck, USA), a PI3K inhibitor, was utilized to investigate the role of the PI3K/Akt signaling pathway in RAPA-sEV-induced anti-inflammatory and pro-angiogenic effects.

Techniques: Inhibition, Migration

Journal: Materials Today Bio

Article Title: Rapamycin-induced small extracellular vesicles under GelMA scaffolds facilitate diabetic wound repair through accelerating angiogenesis and alleviating macrophage-mediated inflammation via PI3K/Akt signaling pathway

doi: 10.1016/j.mtbio.2025.101846

Figure Lengend Snippet: PI3K/Akt signaling pathway was responsible for RAPA-sEV-induced diabetic wound repair. ( A ) Diabetic mice with full-thickness defects (7 mm) were treated with hydrogel, hydrogel + sEVs2, and hydrogel + sEVs2 + PI103 at postoperative days 0, 4, 9, and 14. ( B ) Quantitative analysis of wound closure rate (%). ( C ) The phosphorylation levels of PI3K and AKT, as well as the relative protein expression levels of wound skin tissues after being treated with PI103 by Western blotting. ( D ) Quantitative analysis of Western blotting assays. ( E ) The relative mRNA expressions of inflammation-related factors (TNF-α and IL-1β) and angiogenesis-related markers (PECAM-1 and VEGF) after treatment with PI103. Mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: PI-103 (S1038, Selleck, USA), a PI3K inhibitor, was utilized to investigate the role of the PI3K/Akt signaling pathway in RAPA-sEV-induced anti-inflammatory and pro-angiogenic effects.

Techniques: Phospho-proteomics, Expressing, Western Blot