stat3 mouse cell signaling Search Results


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Fig. 5. Au@PSMA-Sit NPs promote M1 polarization via endocytosis-induced ER stress-mediated SYK activation in LLC TAMs. (a) The Z-axis imaging of LLC TAMs pre-treated with each endocytosis inhibitor (Rottlerin, Chlorpromazine, and Genistein) for 4 h, then treated with Au@PSMA-Sit-FITC NPs for another 24 h (Scale bar, 10 µm). (b) Violin plot of ER stress signature genes with normalized expression scores in macrophage cluster of Au@PSMA-Sit NPs group compared with sitravatinib group. (c) The co-localization of dark field signals (green) and ER component (red) in LLC TAMs pre-treated with caveolae-mediated endocytosis inhibitor (Genistein) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h (Scale bar, 50 µm). (d) The expression of total/phosphor- EIF2A, SYK, NF-κB, <t>STAT3,</t> and STAT6 in LLC TAMs treated with Au@PSMA-Sit for 24 h using western blot and (e) flow cytometry. (f) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and (g) the proportion of M1 phenotype (F4/80+CD86+) and M2 phenotype (F4/80+CD206+) in LLC TAMs after pre-treated with caveolae-mediated endocytosis inhibitor (Genistein), ER stress inhibitor (4μ8C and GSK2606414) and SYK kinase inhibitor (Piceatannol and R406) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h. The error bars represent SD (One-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001).
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Fig. 5. Au@PSMA-Sit NPs promote M1 polarization via endocytosis-induced ER stress-mediated SYK activation in LLC TAMs. (a) The Z-axis imaging of LLC TAMs pre-treated with each endocytosis inhibitor (Rottlerin, Chlorpromazine, and Genistein) for 4 h, then treated with Au@PSMA-Sit-FITC NPs for another 24 h (Scale bar, 10 µm). (b) Violin plot of ER stress signature genes with normalized expression scores in macrophage cluster of Au@PSMA-Sit NPs group compared with sitravatinib group. (c) The co-localization of dark field signals (green) and ER component (red) in LLC TAMs pre-treated with caveolae-mediated endocytosis inhibitor (Genistein) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h (Scale bar, 50 µm). (d) The expression of total/phosphor- EIF2A, SYK, NF-κB, <t>STAT3,</t> and STAT6 in LLC TAMs treated with Au@PSMA-Sit for 24 h using western blot and (e) flow cytometry. (f) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and (g) the proportion of M1 phenotype (F4/80+CD86+) and M2 phenotype (F4/80+CD206+) in LLC TAMs after pre-treated with caveolae-mediated endocytosis inhibitor (Genistein), ER stress inhibitor (4μ8C and GSK2606414) and SYK kinase inhibitor (Piceatannol and R406) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h. The error bars represent SD (One-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001).
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Fig. 1 | PRMT5 expression levels are increased in lung cancer cells. a, b PRMT5 expression is elevated in a lung adenocarcinoma and b lung squamous cell carci- noma. RNA-seq data from The Cancer Genome Atlas (TCGA) were analysed on the UCSC Xena browser. c Correlation between <t>STAT3</t> and PRMT5 protein levels in 12 NSCLC cell lines (NCI-H23, LU65, CORL105, CHAGOK1, NCI-H3255, NCI-
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Fig. 1 | PRMT5 expression levels are increased in lung cancer cells. a, b PRMT5 expression is elevated in a lung adenocarcinoma and b lung squamous cell carci- noma. RNA-seq data from The Cancer Genome Atlas (TCGA) were analysed on the UCSC Xena browser. c Correlation between <t>STAT3</t> and PRMT5 protein levels in 12 NSCLC cell lines (NCI-H23, LU65, CORL105, CHAGOK1, NCI-H3255, NCI-
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Fig. 1 | PRMT5 expression levels are increased in lung cancer cells. a, b PRMT5 expression is elevated in a lung adenocarcinoma and b lung squamous cell carci- noma. RNA-seq data from The Cancer Genome Atlas (TCGA) were analysed on the UCSC Xena browser. c Correlation between <t>STAT3</t> and PRMT5 protein levels in 12 NSCLC cell lines (NCI-H23, LU65, CORL105, CHAGOK1, NCI-H3255, NCI-
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Image Search Results


Fig. 5. Au@PSMA-Sit NPs promote M1 polarization via endocytosis-induced ER stress-mediated SYK activation in LLC TAMs. (a) The Z-axis imaging of LLC TAMs pre-treated with each endocytosis inhibitor (Rottlerin, Chlorpromazine, and Genistein) for 4 h, then treated with Au@PSMA-Sit-FITC NPs for another 24 h (Scale bar, 10 µm). (b) Violin plot of ER stress signature genes with normalized expression scores in macrophage cluster of Au@PSMA-Sit NPs group compared with sitravatinib group. (c) The co-localization of dark field signals (green) and ER component (red) in LLC TAMs pre-treated with caveolae-mediated endocytosis inhibitor (Genistein) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h (Scale bar, 50 µm). (d) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and STAT6 in LLC TAMs treated with Au@PSMA-Sit for 24 h using western blot and (e) flow cytometry. (f) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and (g) the proportion of M1 phenotype (F4/80+CD86+) and M2 phenotype (F4/80+CD206+) in LLC TAMs after pre-treated with caveolae-mediated endocytosis inhibitor (Genistein), ER stress inhibitor (4μ8C and GSK2606414) and SYK kinase inhibitor (Piceatannol and R406) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h. The error bars represent SD (One-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001).

Journal: Nano Today

Article Title: Polymeric nano-formulation of spectrum selective RTK inhibitor strengthens anti-cancer effects via immune remodeling by endoplasmic reticulum stress-modulating mitochondrial metabolism

doi: 10.1016/j.nantod.2023.102070

Figure Lengend Snippet: Fig. 5. Au@PSMA-Sit NPs promote M1 polarization via endocytosis-induced ER stress-mediated SYK activation in LLC TAMs. (a) The Z-axis imaging of LLC TAMs pre-treated with each endocytosis inhibitor (Rottlerin, Chlorpromazine, and Genistein) for 4 h, then treated with Au@PSMA-Sit-FITC NPs for another 24 h (Scale bar, 10 µm). (b) Violin plot of ER stress signature genes with normalized expression scores in macrophage cluster of Au@PSMA-Sit NPs group compared with sitravatinib group. (c) The co-localization of dark field signals (green) and ER component (red) in LLC TAMs pre-treated with caveolae-mediated endocytosis inhibitor (Genistein) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h (Scale bar, 50 µm). (d) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and STAT6 in LLC TAMs treated with Au@PSMA-Sit for 24 h using western blot and (e) flow cytometry. (f) The expression of total/phosphor- EIF2A, SYK, NF-κB, STAT3, and (g) the proportion of M1 phenotype (F4/80+CD86+) and M2 phenotype (F4/80+CD206+) in LLC TAMs after pre-treated with caveolae-mediated endocytosis inhibitor (Genistein), ER stress inhibitor (4μ8C and GSK2606414) and SYK kinase inhibitor (Piceatannol and R406) for 4 h, then treated with Au@PSMA-Sit NPs for another 24 h. The error bars represent SD (One-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001).

Article Snippet: The following antibodies were used for western blot analysis: Phospho-AXL (#PA5–64862, Thermo Fisher Scientific), AXL (#13196–1-AP, Proteintech), Phospho-MerTK (#NB300–690, Novus Biologicals), MerTK (#AF591, R&D Systems), Tyro3 (#5585 S, Cell Signaling Technology), Phospho-p38 MAPK (#4511 S, Cell Signaling Technology), p38 MAPK (#8690 S, Cell Signaling Technology), Phospho-p44/42 MAPK (#9101 S, Cell Signaling Technology), p44/42 MAPK (#4695 S, Cell Signaling Technology), Phospho-Stat3 (#9145 S, Cell Signaling Technology), Stat3 (#9139 S, Cell Signaling Technology), Phospho-Akt (#4060 S, Cell Signaling Technology), Akt (#9272 S, Cell Signaling Technology), Phospho-eIF2α (#3398 S, Cell Signaling Technology), eIF2α (#5324 S, Cell Signaling Technology), Phospho-SYK (#ab278675, Abcam), SYK (#13198 S, Cell Signaling Technology), Phospho-NF-κB p65 (#3033 S, Cell Signaling Technology), NF-κB p65 (#8242 S, Cell Signaling Technology), Phospho-DRP1 (#4867 S, Cell Signaling Technology), DRP1 (#12957–1-AP, Proteintech), FIS1 (#10956–1-AP, Proteintech), MFN1 (#13798–1-AP, Proteintech), OPA1 (#27733–1-AP, Proteintech), HSP70 (#4872 S, Cell Signaling Technology), HSP90 (#4877 S, Cell Signaling Technology), HMGB1 (#3935 S, Cell Signaling Technology), and CRT (#12238 S, Cell Signaling Technology).

Techniques: Activation Assay, Imaging, Expressing, Western Blot, Flow Cytometry

Fig. 1 | PRMT5 expression levels are increased in lung cancer cells. a, b PRMT5 expression is elevated in a lung adenocarcinoma and b lung squamous cell carci- noma. RNA-seq data from The Cancer Genome Atlas (TCGA) were analysed on the UCSC Xena browser. c Correlation between STAT3 and PRMT5 protein levels in 12 NSCLC cell lines (NCI-H23, LU65, CORL105, CHAGOK1, NCI-H3255, NCI-

Journal: Communications biology

Article Title: PRMT5-mediated methylation of STAT3 is required for lung cancer stem cell maintenance and tumour growth.

doi: 10.1038/s42003-024-06290-7

Figure Lengend Snippet: Fig. 1 | PRMT5 expression levels are increased in lung cancer cells. a, b PRMT5 expression is elevated in a lung adenocarcinoma and b lung squamous cell carci- noma. RNA-seq data from The Cancer Genome Atlas (TCGA) were analysed on the UCSC Xena browser. c Correlation between STAT3 and PRMT5 protein levels in 12 NSCLC cell lines (NCI-H23, LU65, CORL105, CHAGOK1, NCI-H3255, NCI-

Article Snippet: STAT3 activation was monitored by western blotting using an anti-phosphorylated STAT3 (Y705) antibody (CST; 9138).

Techniques: Expressing, RNA Sequencing