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R&D Systems recombinant human sgp130 fc
IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus <t>sgp130-Fc</t> or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
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1) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

Journal: bioRxiv

doi: 10.1101/2020.05.28.121145

IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
Figure Legend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

Techniques Used: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P
Figure Legend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

Techniques Used: Cell Culture, Blocking Assay

2) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

Journal: bioRxiv

doi: 10.1101/2020.05.28.121145

IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
Figure Legend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

Techniques Used: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P
Figure Legend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

Techniques Used: Cell Culture, Blocking Assay

3) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during clinical latency

Journal: Nature Communications

doi: 10.1038/s41467-020-18701-4

IL6 trans-signaling regulates sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence ( n = 18) or presence of IL6 ( n = 18), an IL6-blocking antibody ( n = 6) or hyper-IL6 ( n = 6). b hTERT-HME1 were cultured as spheres in the absence ( n = 3) or presence ( n = 3) of hyper-IL6. c HMECs were cultured as spheres without or with IL6, with an IL6 blocking antibody or hyper-IL6. n = 3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR∆746-750 cells were cultured as spheres in the absence or presence of HIL6 (each n = 12). e MCF 10A cells were cultured as spheres without ( n = 6) or with IL6 ( n = 6) and IL6 plus sgp130-Fc at indicated concentrations (each n = 6). f Sphere formation of hTERT-HME1-EGFR∆746-750 in the absence ( n = 10) or presence of an anti-IL6 antibody ( n = 9) or with sgp130-Fc at indicated concentrations (each n = 12). Cumulative data of three experiments. P values in a , c , f : one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); b , d two-sided Student’s t-test; e one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (**** p
Figure Legend Snippet: IL6 trans-signaling regulates sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence ( n = 18) or presence of IL6 ( n = 18), an IL6-blocking antibody ( n = 6) or hyper-IL6 ( n = 6). b hTERT-HME1 were cultured as spheres in the absence ( n = 3) or presence ( n = 3) of hyper-IL6. c HMECs were cultured as spheres without or with IL6, with an IL6 blocking antibody or hyper-IL6. n = 3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR∆746-750 cells were cultured as spheres in the absence or presence of HIL6 (each n = 12). e MCF 10A cells were cultured as spheres without ( n = 6) or with IL6 ( n = 6) and IL6 plus sgp130-Fc at indicated concentrations (each n = 6). f Sphere formation of hTERT-HME1-EGFR∆746-750 in the absence ( n = 10) or presence of an anti-IL6 antibody ( n = 9) or with sgp130-Fc at indicated concentrations (each n = 12). Cumulative data of three experiments. P values in a , c , f : one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); b , d two-sided Student’s t-test; e one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (**** p

Techniques Used: Cell Culture, Blocking Assay

4) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

Journal: bioRxiv

doi: 10.1101/2020.05.28.121145

IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
Figure Legend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

Techniques Used: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P
Figure Legend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

Techniques Used: Cell Culture, Blocking Assay

5) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during clinical latency

Journal: Nature Communications

doi: 10.1038/s41467-020-18701-4

IL6 trans-signaling regulates sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence ( n = 18) or presence of IL6 ( n = 18), an IL6-blocking antibody ( n = 6) or hyper-IL6 ( n = 6). b hTERT-HME1 were cultured as spheres in the absence ( n = 3) or presence ( n = 3) of hyper-IL6. c HMECs were cultured as spheres without or with IL6, with an IL6 blocking antibody or hyper-IL6. n = 3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR∆746-750 cells were cultured as spheres in the absence or presence of HIL6 (each n = 12). e MCF 10A cells were cultured as spheres without ( n = 6) or with IL6 ( n = 6) and IL6 plus sgp130-Fc at indicated concentrations (each n = 6). f Sphere formation of hTERT-HME1-EGFR∆746-750 in the absence ( n = 10) or presence of an anti-IL6 antibody ( n = 9) or with sgp130-Fc at indicated concentrations (each n = 12). Cumulative data of three experiments. P values in a , c , f : one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); b , d two-sided Student’s t-test; e one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (**** p
Figure Legend Snippet: IL6 trans-signaling regulates sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence ( n = 18) or presence of IL6 ( n = 18), an IL6-blocking antibody ( n = 6) or hyper-IL6 ( n = 6). b hTERT-HME1 were cultured as spheres in the absence ( n = 3) or presence ( n = 3) of hyper-IL6. c HMECs were cultured as spheres without or with IL6, with an IL6 blocking antibody or hyper-IL6. n = 3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR∆746-750 cells were cultured as spheres in the absence or presence of HIL6 (each n = 12). e MCF 10A cells were cultured as spheres without ( n = 6) or with IL6 ( n = 6) and IL6 plus sgp130-Fc at indicated concentrations (each n = 6). f Sphere formation of hTERT-HME1-EGFR∆746-750 in the absence ( n = 10) or presence of an anti-IL6 antibody ( n = 9) or with sgp130-Fc at indicated concentrations (each n = 12). Cumulative data of three experiments. P values in a , c , f : one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); b , d two-sided Student’s t-test; e one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (**** p

Techniques Used: Cell Culture, Blocking Assay

6) Product Images from "Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency"

Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

Journal: bioRxiv

doi: 10.1101/2020.05.28.121145

IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
Figure Legend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

Techniques Used: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P
Figure Legend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

Techniques Used: Cell Culture, Blocking Assay

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    R&D Systems recombinant human gp130 fc chimera protein cf
    IL11RA is highly expressed in hepatocytes and IL11 cis -signaling is hepatotoxic. a Immunohistochemistry staining of IL11RA and IL6R in healthy human liver sections (scale bars, 20 µm, n = 1 independent experiment, due to limited amount of human liver section). b Flow cytometry forward scatter (FSC) plots of IL11RA, IL6R, and <t>gp130</t> staining and fluorescence intensity plots of IL11RA and IL6R staining on hepatocytes and THP-1. c Abundance of IL11RA1 and IL6R reads in hepatocytes at baseline based on RNA-seq (left) and Ribo-seq (right) (transcripts per million, TPM) ( n = 3). d , e Read coverage of d IL11RA1 and e IL6R transcripts based on RNA-seq (gray) and Ribo-seq (red) of primary human hepatocytes ( n = 3). f Western blots showing ERK, JNK, and STAT3 activation status and g ALT secretion ( n = 4) by hepatocytes following a dose range stimulation of either hyperIL11 or hyperIL6. h ALT levels in the supernatants of hepatocytes stimulated with hyperIL11 alone or in the presence of increasing amounts of soluble gp130 (sgp130) ( n = 4). i , j Western blots of hepatocyte lysates showing i phosphorylated ERK and JNK and their respective total expression in response to hyperIL11 stimulation alone or with sgp130 and j phospho-STAT3 and total STAT3 in response to hyperIL6 stimulation with and without sgp130. k Representative FSC plots of propidium Iodide (PI) staining of IL11-stimulated hepatocytes in the presence of sgp130 or soluble IL11RA (sIL11RA). l Western blots showing phospho-ERK, phospho-JNK, cleaved caspase-3, and their respective total expression, NOX4, and GAPDH in hepatocytes in response to IL11 stimulation alone or in the presence of sgp130 or sIL11RA. i , j , l Representative data of n = 2 independent experiments. b – l Primary human hepatocytes; f – l 24 h stimulation; hyperIL11, hyperIL6, IL11 (20 ng/ml), sgp130, sIL11RA (1 µg/ml). c , g , h Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and min–max values (whiskers). g , h One-way ANOVA with Dunnett’s correction. Source data are provided as a Source data file.
    Recombinant Human Gp130 Fc Chimera Protein Cf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant human sgp130 fc
    IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus <t>sgp130-Fc</t> or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
    Recombinant Human Sgp130 Fc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    IL11RA is highly expressed in hepatocytes and IL11 cis -signaling is hepatotoxic. a Immunohistochemistry staining of IL11RA and IL6R in healthy human liver sections (scale bars, 20 µm, n = 1 independent experiment, due to limited amount of human liver section). b Flow cytometry forward scatter (FSC) plots of IL11RA, IL6R, and gp130 staining and fluorescence intensity plots of IL11RA and IL6R staining on hepatocytes and THP-1. c Abundance of IL11RA1 and IL6R reads in hepatocytes at baseline based on RNA-seq (left) and Ribo-seq (right) (transcripts per million, TPM) ( n = 3). d , e Read coverage of d IL11RA1 and e IL6R transcripts based on RNA-seq (gray) and Ribo-seq (red) of primary human hepatocytes ( n = 3). f Western blots showing ERK, JNK, and STAT3 activation status and g ALT secretion ( n = 4) by hepatocytes following a dose range stimulation of either hyperIL11 or hyperIL6. h ALT levels in the supernatants of hepatocytes stimulated with hyperIL11 alone or in the presence of increasing amounts of soluble gp130 (sgp130) ( n = 4). i , j Western blots of hepatocyte lysates showing i phosphorylated ERK and JNK and their respective total expression in response to hyperIL11 stimulation alone or with sgp130 and j phospho-STAT3 and total STAT3 in response to hyperIL6 stimulation with and without sgp130. k Representative FSC plots of propidium Iodide (PI) staining of IL11-stimulated hepatocytes in the presence of sgp130 or soluble IL11RA (sIL11RA). l Western blots showing phospho-ERK, phospho-JNK, cleaved caspase-3, and their respective total expression, NOX4, and GAPDH in hepatocytes in response to IL11 stimulation alone or in the presence of sgp130 or sIL11RA. i , j , l Representative data of n = 2 independent experiments. b – l Primary human hepatocytes; f – l 24 h stimulation; hyperIL11, hyperIL6, IL11 (20 ng/ml), sgp130, sIL11RA (1 µg/ml). c , g , h Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and min–max values (whiskers). g , h One-way ANOVA with Dunnett’s correction. Source data are provided as a Source data file.

    Journal: Nature Communications

    Article Title: Hepatocyte-specific IL11 cis-signaling drives lipotoxicity and underlies the transition from NAFLD to NASH

    doi: 10.1038/s41467-020-20303-z

    Figure Lengend Snippet: IL11RA is highly expressed in hepatocytes and IL11 cis -signaling is hepatotoxic. a Immunohistochemistry staining of IL11RA and IL6R in healthy human liver sections (scale bars, 20 µm, n = 1 independent experiment, due to limited amount of human liver section). b Flow cytometry forward scatter (FSC) plots of IL11RA, IL6R, and gp130 staining and fluorescence intensity plots of IL11RA and IL6R staining on hepatocytes and THP-1. c Abundance of IL11RA1 and IL6R reads in hepatocytes at baseline based on RNA-seq (left) and Ribo-seq (right) (transcripts per million, TPM) ( n = 3). d , e Read coverage of d IL11RA1 and e IL6R transcripts based on RNA-seq (gray) and Ribo-seq (red) of primary human hepatocytes ( n = 3). f Western blots showing ERK, JNK, and STAT3 activation status and g ALT secretion ( n = 4) by hepatocytes following a dose range stimulation of either hyperIL11 or hyperIL6. h ALT levels in the supernatants of hepatocytes stimulated with hyperIL11 alone or in the presence of increasing amounts of soluble gp130 (sgp130) ( n = 4). i , j Western blots of hepatocyte lysates showing i phosphorylated ERK and JNK and their respective total expression in response to hyperIL11 stimulation alone or with sgp130 and j phospho-STAT3 and total STAT3 in response to hyperIL6 stimulation with and without sgp130. k Representative FSC plots of propidium Iodide (PI) staining of IL11-stimulated hepatocytes in the presence of sgp130 or soluble IL11RA (sIL11RA). l Western blots showing phospho-ERK, phospho-JNK, cleaved caspase-3, and their respective total expression, NOX4, and GAPDH in hepatocytes in response to IL11 stimulation alone or in the presence of sgp130 or sIL11RA. i , j , l Representative data of n = 2 independent experiments. b – l Primary human hepatocytes; f – l 24 h stimulation; hyperIL11, hyperIL6, IL11 (20 ng/ml), sgp130, sIL11RA (1 µg/ml). c , g , h Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and min–max values (whiskers). g , h One-way ANOVA with Dunnett’s correction. Source data are provided as a Source data file.

    Article Snippet: Recombinant proteinsCommercial recombinant proteins: Human hyperIL6 (IL6R:IL6 fusion protein, 8954-SR, R & D Systems), human IL6 (206-IL-010, R & D Systems), human soluble gp130 Fc (671-GP-100, R & D Systems), human IL11RA (8895-MR-050, R & D Systems).

    Techniques: Immunohistochemistry, Staining, Flow Cytometry, Fluorescence, RNA Sequencing Assay, Western Blot, Activation Assay, Expressing, Whisker Assay

    ELISA analysis of soluble OSMR and soluble LIFR binding with LIF, OSM-WT, OSM-M1, and OSM-M2 or gp130-bound LIF (gp130-LIF), OSM-WT (gp130-OSM-WT), OSM-M1 (gp130-OSM-M1), and OSM-M2 (gp130-OSM-M2). Cytokines (LIF, OSM-WT, OSM-M1, or OSM-M2) immobilized

    Journal: The Journal of Biological Chemistry

    Article Title: A Unique Loop Structure in Oncostatin M Determines Binding Affinity toward Oncostatin M Receptor and Leukemia Inhibitory Factor Receptor *

    doi: 10.1074/jbc.M112.387324

    Figure Lengend Snippet: ELISA analysis of soluble OSMR and soluble LIFR binding with LIF, OSM-WT, OSM-M1, and OSM-M2 or gp130-bound LIF (gp130-LIF), OSM-WT (gp130-OSM-WT), OSM-M1 (gp130-OSM-M1), and OSM-M2 (gp130-OSM-M2). Cytokines (LIF, OSM-WT, OSM-M1, or OSM-M2) immobilized

    Article Snippet: For interactions of a higher order, soluble human gp130 (catalog no. 671-GP-100, R & D Systems) was immobilized on 96-well ELISA microplates by incubating the wells with 200 μl of 1 n m gp130 solution (in PBS (pH 7.4)) overnight at 4 °C.

    Techniques: Enzyme-linked Immunosorbent Assay, Binding Assay

    Kinetic analysis of soluble LIFR and soluble gp130 interaction with LIF, OSM-WT, OSM-M1, or OSM-M2. Soluble LIFR ( left panels ) or soluble gp130 ( right panels ) at various concentrations were injected over an SPR sensor chip with immobilized ligand (LIF,

    Journal: The Journal of Biological Chemistry

    Article Title: A Unique Loop Structure in Oncostatin M Determines Binding Affinity toward Oncostatin M Receptor and Leukemia Inhibitory Factor Receptor *

    doi: 10.1074/jbc.M112.387324

    Figure Lengend Snippet: Kinetic analysis of soluble LIFR and soluble gp130 interaction with LIF, OSM-WT, OSM-M1, or OSM-M2. Soluble LIFR ( left panels ) or soluble gp130 ( right panels ) at various concentrations were injected over an SPR sensor chip with immobilized ligand (LIF,

    Article Snippet: For interactions of a higher order, soluble human gp130 (catalog no. 671-GP-100, R & D Systems) was immobilized on 96-well ELISA microplates by incubating the wells with 200 μl of 1 n m gp130 solution (in PBS (pH 7.4)) overnight at 4 °C.

    Techniques: Injection, SPR Assay, Chromatin Immunoprecipitation

    IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Article Snippet: For some analyses mammosphere media was supplemented additionally with 10 ng/ml IL6 (Sigma-Aldrich, Germany), 1.5 µg/ml anti-IL6 antibody (Sigma-Aldrich, Germany), 20 ng/ml Hyper-IL6, 0.1 or 10 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany).

    Techniques: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

    IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Article Snippet: For some analyses mammosphere media was supplemented additionally with 10 ng/ml IL6 (Sigma-Aldrich, Germany), 1.5 µg/ml anti-IL6 antibody (Sigma-Aldrich, Germany), 20 ng/ml Hyper-IL6, 0.1 or 10 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany).

    Techniques: Cell Culture, Blocking Assay

    IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Article Snippet: mRNA microarray experimentsMCF 10A cells were cultured as mammospheres in the presence or absence of 10 ng/ml IL6 (Sigma-Aldrich, Germany), 10 ng/ml IL6 + 0.1 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany) or 20 ng/ml Hyper-IL6 (kind gift of S. Rose-John, Christian-Albrechts-University, Germany) for 12 and 24 hours.

    Techniques: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

    IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Article Snippet: mRNA microarray experimentsMCF 10A cells were cultured as mammospheres in the presence or absence of 10 ng/ml IL6 (Sigma-Aldrich, Germany), 10 ng/ml IL6 + 0.1 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany) or 20 ng/ml Hyper-IL6 (kind gift of S. Rose-John, Christian-Albrechts-University, Germany) for 12 and 24 hours.

    Techniques: Cell Culture, Blocking Assay