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OGD/R induces early activation of ER stress sensors followed by apoptosis in cultured cortical neurons, which is ameliorated by ER stress inhibitors. (A) Schematic representation of the timeline of the experimental procedures. Cortical neurons (7 DIV) were cultured in normal conditions (Control group) or exposed to oxygen/glucose deprivation for 4 hours followed by reperfusion (OGD/R group). Cell lysates were collected at various time points for Western blotting, and cell viability was evaluated after 24 hours reperfusion. (B) The cell viability of primary cortical neurons after OGD/R 24 hours was detected by MTT assay. Cortical neurons (7 DIV) under standard culture conditions were used as the control group ( n = 3). ** P < 0.01, vs. control, unpaired t -test. (C) Cell lysates from the OGD/R group were collected at different time points (0–24 hours) after reperfusion. For the control group, cell lysates were collected at the same time corresponding to 0 hours reperfusion of OGD/R group. Levels of ER stress sensors, protein synthesis, and apoptosis-related proteins were examined by western blot analysis. (D–K) Quantifications of the normalized levels of <t>p-PERK/PERK</t> (D, n = 4), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 3), CHOP (J, n = 3), and cleaved-caspase-3 (K, n = 3). GAPDH and α-tubulin served as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, vs . control, one-way analysis of variance followed by Dunnett’s multiple comparison test. (L) A schematic illustration of the application of ER stress inhibitors, sodium 4-PBA or Sal, to neurons 1 hour before OGD and during OGD (−5 to 0 hours). (M, N) MTT assay was performed to evaluate cell viability of neurons treated with 4-PBA or Sal ( n = 3). **** P < 0.0001, OGD/R vs. control; # P < 0.05, ## P < 0.01, 4-PBA (50 or 100 µM) or Sal (25 or 100 µM) vs. OGD/R, unpaired t -test. Data are shown as mean ± SEM. 4-PBA: Sodium 4-phenylbutyrate; ATF: activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; MTT: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: <t>phosphorylated-;</t> PERK: double-stranded RNA-activated protein kinase-like ER kinase; Sal: salubrinal.

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1) Product Images from "Neuroserpin alleviates cerebral ischemia-reperfusion injury by suppressing ischemia-induced endoplasmic reticulum stress"

Article Title: Neuroserpin alleviates cerebral ischemia-reperfusion injury by suppressing ischemia-induced endoplasmic reticulum stress

Journal: Neural Regeneration Research

doi: 10.4103/NRR.NRR-D-24-00044

Figure Legend Snippet: OGD/R induces early activation of ER stress sensors followed by apoptosis in cultured cortical neurons, which is ameliorated by ER stress inhibitors. (A) Schematic representation of the timeline of the experimental procedures. Cortical neurons (7 DIV) were cultured in normal conditions (Control group) or exposed to oxygen/glucose deprivation for 4 hours followed by reperfusion (OGD/R group). Cell lysates were collected at various time points for Western blotting, and cell viability was evaluated after 24 hours reperfusion. (B) The cell viability of primary cortical neurons after OGD/R 24 hours was detected by MTT assay. Cortical neurons (7 DIV) under standard culture conditions were used as the control group ( n = 3). ** P < 0.01, vs. control, unpaired t -test. (C) Cell lysates from the OGD/R group were collected at different time points (0–24 hours) after reperfusion. For the control group, cell lysates were collected at the same time corresponding to 0 hours reperfusion of OGD/R group. Levels of ER stress sensors, protein synthesis, and apoptosis-related proteins were examined by western blot analysis. (D–K) Quantifications of the normalized levels of p-PERK/PERK (D, n = 4), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 3), CHOP (J, n = 3), and cleaved-caspase-3 (K, n = 3). GAPDH and α-tubulin served as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, vs . control, one-way analysis of variance followed by Dunnett’s multiple comparison test. (L) A schematic illustration of the application of ER stress inhibitors, sodium 4-PBA or Sal, to neurons 1 hour before OGD and during OGD (−5 to 0 hours). (M, N) MTT assay was performed to evaluate cell viability of neurons treated with 4-PBA or Sal ( n = 3). **** P < 0.0001, OGD/R vs. control; # P < 0.05, ## P < 0.01, 4-PBA (50 or 100 µM) or Sal (25 or 100 µM) vs. OGD/R, unpaired t -test. Data are shown as mean ± SEM. 4-PBA: Sodium 4-phenylbutyrate; ATF: activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; MTT: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: phosphorylated-; PERK: double-stranded RNA-activated protein kinase-like ER kinase; Sal: salubrinal.

Techniques Used: Activation Assay, Cell Culture, Control, Western Blot, MTT Assay, Comparison, Binding Assay, In Vitro

Neuroserpin inhibits ER stress–mediated signaling transduction induced by OGD/R. (A) Schematic representation of the timing of the experimental procedures. Neuroserpin (NSP; 20 ng/mL) was added to cortical neurons (7 DIV) 4 hours before OGD and during OGD, followed by reperfusion. Cell lysates were collected at the indicated time points of reperfusion for the examination of ER stress signaling molecules. (B) Representative western blots showing phosphorylated and total levels of ER stress sensors and apoptosis-related proteins. (C) Representative western blots showing levels of puromycin. (D–K) Quantitative analysis of the normalized p-PERK/PERK (D, n = 3), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 5), CHOP (J, n = 5), and cleaved-caspase-3 (K, n = 4). GAPDH and α-tubulin were used as loading controls. ** P < 0.01, *** P < 0.001, OGD/R vs . control; # P < 0.05, ## P < 0.01, OGD/R + NSP vs . OGD/R, unpaired t -test. Data are shown as mean ± SEM. ATF: Activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; i.c.v.: intracerebroventricular; NSP: neuroserpin; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: phosphorylated-; PERK: double-stranded RNA-activated protein kinase-like ER kinase.

Figure Legend Snippet: Neuroserpin inhibits ER stress–mediated signaling transduction induced by OGD/R. (A) Schematic representation of the timing of the experimental procedures. Neuroserpin (NSP; 20 ng/mL) was added to cortical neurons (7 DIV) 4 hours before OGD and during OGD, followed by reperfusion. Cell lysates were collected at the indicated time points of reperfusion for the examination of ER stress signaling molecules. (B) Representative western blots showing phosphorylated and total levels of ER stress sensors and apoptosis-related proteins. (C) Representative western blots showing levels of puromycin. (D–K) Quantitative analysis of the normalized p-PERK/PERK (D, n = 3), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 5), CHOP (J, n = 5), and cleaved-caspase-3 (K, n = 4). GAPDH and α-tubulin were used as loading controls. ** P < 0.01, *** P < 0.001, OGD/R vs . control; # P < 0.05, ## P < 0.01, OGD/R + NSP vs . OGD/R, unpaired t -test. Data are shown as mean ± SEM. ATF: Activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; i.c.v.: intracerebroventricular; NSP: neuroserpin; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: phosphorylated-; PERK: double-stranded RNA-activated protein kinase-like ER kinase.

Techniques Used: Transduction, Western Blot, Control, Binding Assay, In Vitro

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Journal: Neural Regeneration Research

Article Title: Neuroserpin alleviates cerebral ischemia-reperfusion injury by suppressing ischemia-induced endoplasmic reticulum stress

doi: 10.4103/NRR.NRR-D-24-00044

Figure Lengend Snippet: OGD/R induces early activation of ER stress sensors followed by apoptosis in cultured cortical neurons, which is ameliorated by ER stress inhibitors. (A) Schematic representation of the timeline of the experimental procedures. Cortical neurons (7 DIV) were cultured in normal conditions (Control group) or exposed to oxygen/glucose deprivation for 4 hours followed by reperfusion (OGD/R group). Cell lysates were collected at various time points for Western blotting, and cell viability was evaluated after 24 hours reperfusion. (B) The cell viability of primary cortical neurons after OGD/R 24 hours was detected by MTT assay. Cortical neurons (7 DIV) under standard culture conditions were used as the control group ( n = 3). ** P < 0.01, vs. control, unpaired t -test. (C) Cell lysates from the OGD/R group were collected at different time points (0–24 hours) after reperfusion. For the control group, cell lysates were collected at the same time corresponding to 0 hours reperfusion of OGD/R group. Levels of ER stress sensors, protein synthesis, and apoptosis-related proteins were examined by western blot analysis. (D–K) Quantifications of the normalized levels of p-PERK/PERK (D, n = 4), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 3), CHOP (J, n = 3), and cleaved-caspase-3 (K, n = 3). GAPDH and α-tubulin served as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, vs . control, one-way analysis of variance followed by Dunnett’s multiple comparison test. (L) A schematic illustration of the application of ER stress inhibitors, sodium 4-PBA or Sal, to neurons 1 hour before OGD and during OGD (−5 to 0 hours). (M, N) MTT assay was performed to evaluate cell viability of neurons treated with 4-PBA or Sal ( n = 3). **** P < 0.0001, OGD/R vs. control; # P < 0.05, ## P < 0.01, 4-PBA (50 or 100 µM) or Sal (25 or 100 µM) vs. OGD/R, unpaired t -test. Data are shown as mean ± SEM. 4-PBA: Sodium 4-phenylbutyrate; ATF: activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; MTT: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: phosphorylated-; PERK: double-stranded RNA-activated protein kinase-like ER kinase; Sal: salubrinal.

Article Snippet: The following primary antibodies were used (with an overnight incubation at 4°C): neuroserpin (mouse, 1:1000; Santa Cruz Biotechnology, Cat# sc-48360, RRID: AB_628245), phosphorylated-PERK (p-PERK, rabbit, 1:1000, Cell Signaling Technology, Danvers, MA, USA, Cat# 3179S, RRID: AB_2095853), PERK (rabbit, 1:1000, Cell Signaling Technology, Cat# 3192S, RRID: AB_2095847), phosphorylated-eIF2α (p-eIF2α, rabbit, 1:1000, Cell Signaling Technology, Cat# 3398S, RRID: AB_2096481), eIF2α (rabbit, 1:1000, Cell Signaling Technology, Cat# 9722S, RRID: AB_2230924), phosphorylated-IRE1 (p-IRE1, rabbit, 1:1000, Abcam, Cat# ab48187, RRID: AB_873899), IRE1 (rabbit, 1:1000, Abcam, Cat# ab37037, RRID: AB_775780), ATF6 (rabbit, 1:1000, Abcam, Cat# ab203119, RRID: AB_2650448), ATF4 (rabbit, 1:1000; Cell Signaling Technology, Cat# 11815S, RRID: AB_2616025), CHOP (rabbit, 1:1000, Cell Signaling Technology, Cat# 2895S, RRID: AB_2089254), Cleaved caspase-3 (rabbit, 1:1000, Cell Signaling Technology, Cat# 9664S, RRID: AB_2070042), glyceraldehyde-3-phosphate dehydrogenase (GAPDH, rabbit, 1:2000, Proteintech, Rosemont, IL, USA, Cat# 10494-1-AP, RRID: AB_2263076), and α-tubulin (mouse, 1:2000, Sigma-Aldrich, St. Louis, MO, USA, Cat# T8578, RRID: AB_184122).

Techniques: Activation Assay, Cell Culture, Control, Western Blot, MTT Assay, Comparison, Binding Assay, In Vitro

Journal: Neural Regeneration Research

Article Title: Neuroserpin alleviates cerebral ischemia-reperfusion injury by suppressing ischemia-induced endoplasmic reticulum stress

doi: 10.4103/NRR.NRR-D-24-00044

Figure Lengend Snippet: Neuroserpin inhibits ER stress–mediated signaling transduction induced by OGD/R. (A) Schematic representation of the timing of the experimental procedures. Neuroserpin (NSP; 20 ng/mL) was added to cortical neurons (7 DIV) 4 hours before OGD and during OGD, followed by reperfusion. Cell lysates were collected at the indicated time points of reperfusion for the examination of ER stress signaling molecules. (B) Representative western blots showing phosphorylated and total levels of ER stress sensors and apoptosis-related proteins. (C) Representative western blots showing levels of puromycin. (D–K) Quantitative analysis of the normalized p-PERK/PERK (D, n = 3), p-eIF2α/eIF2α (E, n = 3), p-IRE1/IRE1 (F, n = 3), ATF6 (G, n = 3), puromycin (H, n = 3), ATF4 (I, n = 5), CHOP (J, n = 5), and cleaved-caspase-3 (K, n = 4). GAPDH and α-tubulin were used as loading controls. ** P < 0.01, *** P < 0.001, OGD/R vs . control; # P < 0.05, ## P < 0.01, OGD/R + NSP vs . OGD/R, unpaired t -test. Data are shown as mean ± SEM. ATF: Activating transcription factor; CHOP: CCAAT/enhancer binding protein homologous protein; C-Casp-3: cleaved-caspase-3; DIV: day in vitro ; eIF2α: eukaryotic translation initiation factor 2α; ER: endoplasmic reticulum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IRE1: inositol requiring enzyme 1; i.c.v.: intracerebroventricular; NSP: neuroserpin; OGD: oxygen-glucose deprivation; OGD/R: oxygen-glucose deprivation/reperfusion; p-: phosphorylated-; PERK: double-stranded RNA-activated protein kinase-like ER kinase.

Techniques: Transduction, Western Blot, Control, Binding Assay, In Vitro

PERK is a key factor in promoting CTC cluster survival. (A) Relative mRNA expression levels of UPR‐related genes in single CTCs and CTC clusters isolated from NCG‐MDA‐MB‐231/LM2 (left) and C57BL/6‐B16F10 (right) mouse models ( n = 3). (B) Percentage of Annexin V + single and clustered MDA‐MB‐231/LM2‐CTC (left) and B16F10 (right) cells transfected with siRNAs against PERK and IRE1α and treated with or without thapsigargin ( n = 3). (C) Percentage of Annexin V + clustered MDA‐MB‐231/LM2‐CTC (left) and B16F10 (right) cells treated with AMG44 prior to thapsigargin ( n = 3). (D) Relative PERK expression in single CTCs and CTC clusters isolated from BC patients and PDX mouse models (PDX‐1, PDX‐2, and PDX‐3) ( n = 15 for patients; n = 10 for PDX‐1; n = 8 for PDX‐2 and PDX‐3). (E) Schematic design of the experimental design. MDA‐MB‐231/LM2 cells were orthotopically implanted into mice, and lung metastases were analyzed via IHC at week 4. Representative IHC images of pPERK in lung metastases. The arrow indicates single CTCs; the dashed circle indicates CTC cluster. (F‐I) Representative immunofluorescence images of single CTCs and CTC clusters from a patient and the NCG‐MDA‐MB‐231/LM2 mouse model. Cells were stained for pPERK (red), EGFR (green) (F) or TUNEL (purple) (H), GFP (green) (G) or TUNEL (purple) (I), and DAPI (blue). (J) Schematic design of the experiment (left). MDA‐MB‐231/LM2‐CTC cells were pretreated with Vehicle, MK‐28 or AMG44 and then cultured in suspension for 24 h. Percentage of Annexin V + tumor cell clusters was analyzed by flow cytometry (right) ( n = 5). Results represent mean ± SD. Student's t‐test in A and D, one‐way ANOVA test in B, C, and J. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant. Abbreviations: UPR, unfolded protein response; CTCs, circulating tumor cells; NCG, NOD/ShiLtJGpt‐Prkdc em26Cd52 Il2rg em26Cd22 /Gpt; MDA‐MB‐231/LM2, MDA‐MB‐231 lung metastasis 2; ATF6, activating transcription factor 6; PERK, protein kinase R (PKR)‐like endoplasmic reticulum kinase; IRE1α, inositol‐requiring enzyme 1 alpha; BC, breast cancer; PDX, patient‐derived xenograft; IHC, immunohistochemistry; pPERK, phosphorylated PERK; DAPI, 4′,6‐diamidino‐2‐phenylindole; EGFR, epidermal growth factor receptor; GFP, green fluorescent protein; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling; siRNA, small interfering RNA;ANOVA, analysis of variance.

Journal: Cancer Communications

Article Title: Unfolded protein response kinase PERK supports survival and metastasis of circulating tumor cell clusters via SAM synthesis and H3K4me3‐dependent PDGFB signaling

doi: 10.1002/cac2.70072

Figure Lengend Snippet: PERK is a key factor in promoting CTC cluster survival. (A) Relative mRNA expression levels of UPR‐related genes in single CTCs and CTC clusters isolated from NCG‐MDA‐MB‐231/LM2 (left) and C57BL/6‐B16F10 (right) mouse models ( n = 3). (B) Percentage of Annexin V + single and clustered MDA‐MB‐231/LM2‐CTC (left) and B16F10 (right) cells transfected with siRNAs against PERK and IRE1α and treated with or without thapsigargin ( n = 3). (C) Percentage of Annexin V + clustered MDA‐MB‐231/LM2‐CTC (left) and B16F10 (right) cells treated with AMG44 prior to thapsigargin ( n = 3). (D) Relative PERK expression in single CTCs and CTC clusters isolated from BC patients and PDX mouse models (PDX‐1, PDX‐2, and PDX‐3) ( n = 15 for patients; n = 10 for PDX‐1; n = 8 for PDX‐2 and PDX‐3). (E) Schematic design of the experimental design. MDA‐MB‐231/LM2 cells were orthotopically implanted into mice, and lung metastases were analyzed via IHC at week 4. Representative IHC images of pPERK in lung metastases. The arrow indicates single CTCs; the dashed circle indicates CTC cluster. (F‐I) Representative immunofluorescence images of single CTCs and CTC clusters from a patient and the NCG‐MDA‐MB‐231/LM2 mouse model. Cells were stained for pPERK (red), EGFR (green) (F) or TUNEL (purple) (H), GFP (green) (G) or TUNEL (purple) (I), and DAPI (blue). (J) Schematic design of the experiment (left). MDA‐MB‐231/LM2‐CTC cells were pretreated with Vehicle, MK‐28 or AMG44 and then cultured in suspension for 24 h. Percentage of Annexin V + tumor cell clusters was analyzed by flow cytometry (right) ( n = 5). Results represent mean ± SD. Student's t‐test in A and D, one‐way ANOVA test in B, C, and J. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant. Abbreviations: UPR, unfolded protein response; CTCs, circulating tumor cells; NCG, NOD/ShiLtJGpt‐Prkdc em26Cd52 Il2rg em26Cd22 /Gpt; MDA‐MB‐231/LM2, MDA‐MB‐231 lung metastasis 2; ATF6, activating transcription factor 6; PERK, protein kinase R (PKR)‐like endoplasmic reticulum kinase; IRE1α, inositol‐requiring enzyme 1 alpha; BC, breast cancer; PDX, patient‐derived xenograft; IHC, immunohistochemistry; pPERK, phosphorylated PERK; DAPI, 4′,6‐diamidino‐2‐phenylindole; EGFR, epidermal growth factor receptor; GFP, green fluorescent protein; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling; siRNA, small interfering RNA;ANOVA, analysis of variance.

Article Snippet: Following fixation, the slides were incubated overnight with primary antibodies Ki67 (1:100, 27309‐1‐AP, Proteintech, Wuhan, Hubei, China), epidermal growth factor receptor (EGFR, 1:100, ab30, Abcam, Cambridge, MA, USA), pan‐cytokeratin (CK, 1:100, ab7753, Abcam), CD45 (1:100, ab40763, Abcam), E‐cadherin (1:200, ab287970, Abcam), N‐cadherin (1:200, ab18203, Abcam), phosphorylated PERK (pPERK, 1:100, DF7576, Affinity Biosciences, Nanjing, Jiangsu, China), PDGFB (1:100, ER1914‐92, HUABIO, Hangzhou, Zhejiang, China), phosphorylated PDGFRβ (pPDGFRβ, 1:50, ET1611‐29, HUABIO).

Techniques: Expressing, Isolation, Transfection, Immunofluorescence, Staining, TUNEL Assay, Cell Culture, Suspension, Flow Cytometry, Derivative Assay, Immunohistochemistry, Small Interfering RNA

AMG44 and Imatinib combination therapy can reduce CTC cluster number and inhibit metastasis. (A) Schematic representation of the experimental design. Patient‐derived xenograft (PDX‐1) NCG mice were treated with AMG44, Imatinib, or their combination (intraperitoneally, once every two days). (B‐E) Tumor volumes (B), tumor weight (C), mouse body weight (D) and CTC cluster numbers (E) were monitored over time or assessed at the end of experiment ( n = 5). (F‐H) Representative immunofluorescence images (top) and quantification (bottom) of pPDGFRβ (F), pPERK (G) and TUNEL‐positive cells (H) in CTC clusters of PDX‐1 mouse model ( n = 8). (I) Representative images of patient‐derived CTCs. (J) Quantification of cell viability in patient‐derived CTCs treated with AMG44 and/or Imatinib ( n = 3). Results represent mean ± SD. Two‐way ANOVA test in B and D; one‐way ANOVA test in C, D, E, and J; Student's t‐test in F, G, and H. * P < 0.05; ** P < 0.01; *** P < 0.001. Abbreviations: PDX, Patient‐derived xenograft; NCG, NOD/ShiLtJGpt‐Prkdc em26Cd52 Il2rg em26Cd22 /Gpt; CTCs, Circulating tumor cells; pPDGFRβ, phosphorylated platelet‐derived growth factor receptor beta; pPERK, phosphorylated protein kinase RNA‐like endoplasmic reticulum kinase; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling; ANOVA, analysis of variance.

Journal: Cancer Communications

Article Title: Unfolded protein response kinase PERK supports survival and metastasis of circulating tumor cell clusters via SAM synthesis and H3K4me3‐dependent PDGFB signaling

doi: 10.1002/cac2.70072

Figure Lengend Snippet: AMG44 and Imatinib combination therapy can reduce CTC cluster number and inhibit metastasis. (A) Schematic representation of the experimental design. Patient‐derived xenograft (PDX‐1) NCG mice were treated with AMG44, Imatinib, or their combination (intraperitoneally, once every two days). (B‐E) Tumor volumes (B), tumor weight (C), mouse body weight (D) and CTC cluster numbers (E) were monitored over time or assessed at the end of experiment ( n = 5). (F‐H) Representative immunofluorescence images (top) and quantification (bottom) of pPDGFRβ (F), pPERK (G) and TUNEL‐positive cells (H) in CTC clusters of PDX‐1 mouse model ( n = 8). (I) Representative images of patient‐derived CTCs. (J) Quantification of cell viability in patient‐derived CTCs treated with AMG44 and/or Imatinib ( n = 3). Results represent mean ± SD. Two‐way ANOVA test in B and D; one‐way ANOVA test in C, D, E, and J; Student's t‐test in F, G, and H. * P < 0.05; ** P < 0.01; *** P < 0.001. Abbreviations: PDX, Patient‐derived xenograft; NCG, NOD/ShiLtJGpt‐Prkdc em26Cd52 Il2rg em26Cd22 /Gpt; CTCs, Circulating tumor cells; pPDGFRβ, phosphorylated platelet‐derived growth factor receptor beta; pPERK, phosphorylated protein kinase RNA‐like endoplasmic reticulum kinase; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling; ANOVA, analysis of variance.

Techniques: Derivative Assay, Immunofluorescence, TUNEL Assay

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