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GRB1 suppresses pancreatic cancer progression by targeting <t>the</t> <t>PI3K–AKT</t> signaling pathway. (A) GO enrichment analysis of GRB1–PDAC overlapping targets showing enrichment in kinase regulation and phosphatidylinositol signaling. (B) KEGG enrichment highlighting the PI3K–AKT pathway as the key signaling axis. (C) Western blot showing decreased phosphorylation of PI3K and AKT in GRB1‐treated tumor and liver metastasis tissues. (D, E) Molecular docking and visualization demonstrating stable binding of GRB1 to AKT1 and PIK3CA with strong binding energies. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.
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GRB1 suppresses pancreatic cancer progression by targeting <t>the</t> <t>PI3K–AKT</t> signaling pathway. (A) GO enrichment analysis of GRB1–PDAC overlapping targets showing enrichment in kinase regulation and phosphatidylinositol signaling. (B) KEGG enrichment highlighting the PI3K–AKT pathway as the key signaling axis. (C) Western blot showing decreased phosphorylation of PI3K and AKT in GRB1‐treated tumor and liver metastasis tissues. (D, E) Molecular docking and visualization demonstrating stable binding of GRB1 to AKT1 and PIK3CA with strong binding energies. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.
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Image Search Results


GRB1 suppresses pancreatic cancer progression by targeting the PI3K–AKT signaling pathway. (A) GO enrichment analysis of GRB1–PDAC overlapping targets showing enrichment in kinase regulation and phosphatidylinositol signaling. (B) KEGG enrichment highlighting the PI3K–AKT pathway as the key signaling axis. (C) Western blot showing decreased phosphorylation of PI3K and AKT in GRB1‐treated tumor and liver metastasis tissues. (D, E) Molecular docking and visualization demonstrating stable binding of GRB1 to AKT1 and PIK3CA with strong binding energies. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.

Journal: Food Science & Nutrition

Article Title: Ginsenoside Rb1 From the Functional Food Panax ginseng Suppresses Pancreatic Cancer Progression via Macrophage Reprogramming Through the PI3K ‐ AKT Pathway

doi: 10.1002/fsn3.72468

Figure Lengend Snippet: GRB1 suppresses pancreatic cancer progression by targeting the PI3K–AKT signaling pathway. (A) GO enrichment analysis of GRB1–PDAC overlapping targets showing enrichment in kinase regulation and phosphatidylinositol signaling. (B) KEGG enrichment highlighting the PI3K–AKT pathway as the key signaling axis. (C) Western blot showing decreased phosphorylation of PI3K and AKT in GRB1‐treated tumor and liver metastasis tissues. (D, E) Molecular docking and visualization demonstrating stable binding of GRB1 to AKT1 and PIK3CA with strong binding energies. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.

Article Snippet: Gemcitabine (Solarbio, China, G8970), Ginsenoside Rb1 (Macklin, Shanghai, G742231), Mouse Ki67 (Abclonal, China, A20018); CK19 (Abclonal, China, A25546); SOX2 (Abclonal, China, A19118); Vimentin (Abclonal, China, A19607); Zeb‐1 (Abclonal, China, A5600); E‐cadherin (Abcam, USA, ab40772); AKT (Abclonal, China, AP0637); P‐AKT (Abclonal, China, AP0637); PI3K (Abclonal, China, A27717); P‐PI3K (Abclonal, China, A27717); GAPDH (Abclonal, China, A19056); CD45 (BioLegend, USA, 103106); CD3 (BioLegend, USA, 100219); CD11b (BioLegend, USA, 101224); CD206 (Abclonal, China, A21014); CD206 (BioLegend, USA, 141721); CD163 (BioLegend, USA, 155327); ARG1 (BioLegend, USA, 165804); CD86 (BioLegend, USA, 105013); M‐CSF (MCE, USA, HY‐ P70488 ); IL4 (MCE, USA, HY‐139092); PMA (MCE, USA, HY‐18739); collagenase Type IV (Sigma, USA, C5138); deoxyribonuclease I (Thermo, USA, EN0521); Matrigel (Corning, USA, 354234); Organoid culture medium (Omabio, China, OM12).

Techniques: Analysis, Western Blot, Phospho-proteomics, Docking Assay, Binding Assay

Food‐derived bioactive compound GRB1 inhibits M2 macrophage polarization and pancreatic cancer progression via PI3K–AKT signaling. (A) Schematic of macrophage differentiation and co‐culture workflow. PBMCs or THP‐1 cells were induced to M2 macrophages with IL‐4, with or without GRB1 treatment. GRB1‐treated macrophages were co‐cultured with pancreatic cancer organoids or co‐injected with ASPC1 cells in vivo. (B) qRT–PCR showing reduced expression of M2 markers (CD206, TGFB1, CD115) after GRB1 treatment. (C) Western blot showing that GRB1 inhibited PI3K and AKT phosphorylation in macrophages. (D) Bright‐field images of organoids co‐cultured with control, M2, or GRB1‐treated M2 macrophages, showing reduced growth in the GRB1 group. (E–G) Representative liver images, H&E/IHC staining for CD163 and CD206, and quantification showing that GRB1 decreased M2 macrophage infiltration and liver metastases. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.

Journal: Food Science & Nutrition

Article Title: Ginsenoside Rb1 From the Functional Food Panax ginseng Suppresses Pancreatic Cancer Progression via Macrophage Reprogramming Through the PI3K ‐ AKT Pathway

doi: 10.1002/fsn3.72468

Figure Lengend Snippet: Food‐derived bioactive compound GRB1 inhibits M2 macrophage polarization and pancreatic cancer progression via PI3K–AKT signaling. (A) Schematic of macrophage differentiation and co‐culture workflow. PBMCs or THP‐1 cells were induced to M2 macrophages with IL‐4, with or without GRB1 treatment. GRB1‐treated macrophages were co‐cultured with pancreatic cancer organoids or co‐injected with ASPC1 cells in vivo. (B) qRT–PCR showing reduced expression of M2 markers (CD206, TGFB1, CD115) after GRB1 treatment. (C) Western blot showing that GRB1 inhibited PI3K and AKT phosphorylation in macrophages. (D) Bright‐field images of organoids co‐cultured with control, M2, or GRB1‐treated M2 macrophages, showing reduced growth in the GRB1 group. (E–G) Representative liver images, H&E/IHC staining for CD163 and CD206, and quantification showing that GRB1 decreased M2 macrophage infiltration and liver metastases. Data are presented as mean ± SEM. ns, no significance; * p < 0.01, ** p < 0.001, *** p < 0.0001.

Article Snippet: Gemcitabine (Solarbio, China, G8970), Ginsenoside Rb1 (Macklin, Shanghai, G742231), Mouse Ki67 (Abclonal, China, A20018); CK19 (Abclonal, China, A25546); SOX2 (Abclonal, China, A19118); Vimentin (Abclonal, China, A19607); Zeb‐1 (Abclonal, China, A5600); E‐cadherin (Abcam, USA, ab40772); AKT (Abclonal, China, AP0637); P‐AKT (Abclonal, China, AP0637); PI3K (Abclonal, China, A27717); P‐PI3K (Abclonal, China, A27717); GAPDH (Abclonal, China, A19056); CD45 (BioLegend, USA, 103106); CD3 (BioLegend, USA, 100219); CD11b (BioLegend, USA, 101224); CD206 (Abclonal, China, A21014); CD206 (BioLegend, USA, 141721); CD163 (BioLegend, USA, 155327); ARG1 (BioLegend, USA, 165804); CD86 (BioLegend, USA, 105013); M‐CSF (MCE, USA, HY‐ P70488 ); IL4 (MCE, USA, HY‐139092); PMA (MCE, USA, HY‐18739); collagenase Type IV (Sigma, USA, C5138); deoxyribonuclease I (Thermo, USA, EN0521); Matrigel (Corning, USA, 354234); Organoid culture medium (Omabio, China, OM12).

Techniques: Derivative Assay, Co-culture Assay, Cell Culture, Organoids, Injection, In Vivo, Quantitative RT-PCR, Expressing, Western Blot, Phospho-proteomics, Control, Immunohistochemistry