nr2f6 (Proteintech)

Proteintech nr2f6

(A) Overall survival of melanoma patients with a high- or low-IFNγ signature (see Methods), was determined based on Kaplan-Meier analysis. (B) The percent expression of NRs in indicated cell types was analyzed by scRNAseq of human melanoma tissues ( Tirosh et al ., 2016 ). (C) The percent expression of <t>NR2F6</t> in the indicated cell types was assessed using the same dataset. (D) DepMap ( https://depmap.org/portal/ ) scores indicate effects on cell growth following KO of NRs in human melanoma lines. Each data point indicates a different line.

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Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A) Overall survival of melanoma patients with a high- or low-IFNγ signature (see Methods), was determined based on Kaplan-Meier analysis. (B) The percent expression of NRs in indicated cell types was analyzed by scRNAseq of human melanoma tissues ( Tirosh et al ., 2016 ). (C) The percent expression of NR2F6 in the indicated cell types was assessed using the same dataset. (D) DepMap ( https://depmap.org/portal/ ) scores indicate effects on cell growth following KO of NRs in human melanoma lines. Each data point indicates a different line.

Article Snippet: The following antibodies were used to detect respective proteins: NR2F6 (60117-1-Ig, 60117-2-Ig, Proteintech), NAC1 (#4183, #4420, Cell Signaling), FKBP10 (12172-AP, Proteintech), and V5-tag (7/4, Biolegend).

Techniques: Expressing

(A) B16F10 cells that stably express V5-tagged NR1H3 or NR3C1 were established by transduction with the corresponding lentivirus constructs. Cell lysates were analyzed by immunoblotting with an antibody to V5-tag. (B) Growth of cultured cells established in (A) was assessed in vitro using CellTiter-Glo. Relative difference in luminescence values at days 1 and 3 were calculated based on level of luminescence at day 0, which was defined arbitrarily as 1. (C) Cells were inoculated in C57BL/6 mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at the indicated time points. (D) Growth of control and CRISPR-KO B16F10 cells , as assessed using CellTiter-Glo. (E) Lysates established from mouse tumors were analyzed by immunoblotting of indicated proteins. (F) B16F10 cells stably overexpressing either WT or C112S (DNA-binding mutant) NR2F6 constructs were established by transduction of the corresponding lentiviruses, followed by immunoblotting of cell lysates for the indicated proteins. (G) The growth of the transduced cells in vitro was assessed using CellTiter-Glo, as outlined in (B). (H-J) The transduced cells were inoculated in C57BL/6 mice followed by monitoring tumor volumes and mouse survival at the indicated time points. Data are presented as means ± SD. Statistical significance was assessed by one-way ANOVA with Dunnett’s test (B, D, G), two-way ANOVA with Dunnett’s test (C, H), or by long-rank test (I).

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A) B16F10 cells that stably express V5-tagged NR1H3 or NR3C1 were established by transduction with the corresponding lentivirus constructs. Cell lysates were analyzed by immunoblotting with an antibody to V5-tag. (B) Growth of cultured cells established in (A) was assessed in vitro using CellTiter-Glo. Relative difference in luminescence values at days 1 and 3 were calculated based on level of luminescence at day 0, which was defined arbitrarily as 1. (C) Cells were inoculated in C57BL/6 mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at the indicated time points. (D) Growth of control and CRISPR-KO B16F10 cells , as assessed using CellTiter-Glo. (E) Lysates established from mouse tumors were analyzed by immunoblotting of indicated proteins. (F) B16F10 cells stably overexpressing either WT or C112S (DNA-binding mutant) NR2F6 constructs were established by transduction of the corresponding lentiviruses, followed by immunoblotting of cell lysates for the indicated proteins. (G) The growth of the transduced cells in vitro was assessed using CellTiter-Glo, as outlined in (B). (H-J) The transduced cells were inoculated in C57BL/6 mice followed by monitoring tumor volumes and mouse survival at the indicated time points. Data are presented as means ± SD. Statistical significance was assessed by one-way ANOVA with Dunnett’s test (B, D, G), two-way ANOVA with Dunnett’s test (C, H), or by long-rank test (I).

Techniques: Stable Transfection, Transduction, Construct, Western Blot, Cell Culture, In Vitro, Control, CRISPR, Binding Assay, Mutagenesis

( A) B16F10 cells were transduced with scramble (Scr) shRNA or two shRNAs (#194 and #226) targeting murine Nr2f6. NR2F6 mRNA and protein expression were assessed by qPCR and immunoblotting. (B) Growth of cultured cells described in (A) was assessed in vitro using CellTiter-Glo. Relative fold-differences in luminescence on days 1 and 3 were calculated relative to luminescence on day 0, defined arbitrarily as 1. (C) Cells were then inoculated in C57BL/6 mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at indicated time points. (D-E) Cells established in (A) were engrafted into C57BL6 (D) or NSG (E) mice, and tumor volumes monitored at indicated time points. (F) Nr2f6 KO B16F10 cells were established by CRISPR using specific sgRNA (#492 and #495). NR2F6 mRNA and protein expression were assessed by qPCR and immunoblotting. (G-H) Cells established in (F) were inoculated in C57BL6 (G) or NSG (Ayers et al .) mice, and tumor volumes monitored at indicated time points. (I) YUMM1.7 cells were transduced with scrambled (Scr) shRNA or two shRNAs against Nr2f6 as in (A). mRNA and protein expression were assessed by qPCR and immunoblotting. (J) The growth of cultured YUMM1.7 described in (I) was assessed in vitro using CellTiter-Glo. (K-L) Cells established in (I) were then inoculated in C57BL/6 (K) or NSG (L) mice, and tumor volumes monitored at indicated time points. Data are presented as means ± SD. Statistical significance was assessed by two-way ANOVA with Dunnett’s test for multi-comparison correction.

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: ( A) B16F10 cells were transduced with scramble (Scr) shRNA or two shRNAs (#194 and #226) targeting murine Nr2f6. NR2F6 mRNA and protein expression were assessed by qPCR and immunoblotting. (B) Growth of cultured cells described in (A) was assessed in vitro using CellTiter-Glo. Relative fold-differences in luminescence on days 1 and 3 were calculated relative to luminescence on day 0, defined arbitrarily as 1. (C) Cells were then inoculated in C57BL/6 mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at indicated time points. (D-E) Cells established in (A) were engrafted into C57BL6 (D) or NSG (E) mice, and tumor volumes monitored at indicated time points. (F) Nr2f6 KO B16F10 cells were established by CRISPR using specific sgRNA (#492 and #495). NR2F6 mRNA and protein expression were assessed by qPCR and immunoblotting. (G-H) Cells established in (F) were inoculated in C57BL6 (G) or NSG (Ayers et al .) mice, and tumor volumes monitored at indicated time points. (I) YUMM1.7 cells were transduced with scrambled (Scr) shRNA or two shRNAs against Nr2f6 as in (A). mRNA and protein expression were assessed by qPCR and immunoblotting. (J) The growth of cultured YUMM1.7 described in (I) was assessed in vitro using CellTiter-Glo. (K-L) Cells established in (I) were then inoculated in C57BL/6 (K) or NSG (L) mice, and tumor volumes monitored at indicated time points. Data are presented as means ± SD. Statistical significance was assessed by two-way ANOVA with Dunnett’s test for multi-comparison correction.

Techniques: Transduction, shRNA, Expressing, Western Blot, Cell Culture, In Vitro, CRISPR, Comparison

(A) Heatmaps show Spearman correlation coefficient (left) and corresponding p values (right) for NR2F6 expression (X-axis) in the indicated cancer types [melanoma (SKCM), breast (BRCA), lung (LUAD) and pancreatic (PAAD) cancers) with 10 IFNγ−signature genes (Y-axis). (B) Murine models for the cancer types [B16F10 (SKCM), 4T-1 (BRCA), LLC (LUAD) and KPC (PAAD)] in (A) were transduced with scrambled (Scr) or two shRNAs (#194 and #226) against NR2F6. The KD efficiency was assessed by immunoblotting using indicated antibodies. (C) The growth of transduced cells in vitro was assessed by CellTiter-Glo. Relative fold-differences in luminescence at days 1 and 3 were calculated relative to luminescence on day 0, defined arbitrarily as 1. (D) The transduced cells were inoculated to C57BL/6 (B16F10 and LLC) or BALB/C (4T-1) mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at indicated time points.

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A) Heatmaps show Spearman correlation coefficient (left) and corresponding p values (right) for NR2F6 expression (X-axis) in the indicated cancer types [melanoma (SKCM), breast (BRCA), lung (LUAD) and pancreatic (PAAD) cancers) with 10 IFNγ−signature genes (Y-axis). (B) Murine models for the cancer types [B16F10 (SKCM), 4T-1 (BRCA), LLC (LUAD) and KPC (PAAD)] in (A) were transduced with scrambled (Scr) or two shRNAs (#194 and #226) against NR2F6. The KD efficiency was assessed by immunoblotting using indicated antibodies. (C) The growth of transduced cells in vitro was assessed by CellTiter-Glo. Relative fold-differences in luminescence at days 1 and 3 were calculated relative to luminescence on day 0, defined arbitrarily as 1. (D) The transduced cells were inoculated to C57BL/6 (B16F10 and LLC) or BALB/C (4T-1) mice, which were treated with anti-PD-1 antibody (RMP1-14) at days 6, 9, 12, and 15 (arrows). Tumor volumes were monitored at indicated time points.

Techniques: Expressing, Transduction, Western Blot, In Vitro

(A-B) RNAseq was carried out as described in . Principal component analysis (PCA) of RNAseq data was visualized. (C) Volcano plots visualize up- or down-regulated genes in RNAseq analyses of bulk, MACS-sorted, and cultured cells. (D) The expressions of NR2F6 and NACC1 in human melanoma cell lines (Emran et al .) and human melanoma tissues (TCGA) were assessed. Pearson correlation coefficient ( r ) and corresponding p values ( p )were presented.

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A-B) RNAseq was carried out as described in . Principal component analysis (PCA) of RNAseq data was visualized. (C) Volcano plots visualize up- or down-regulated genes in RNAseq analyses of bulk, MACS-sorted, and cultured cells. (D) The expressions of NR2F6 and NACC1 in human melanoma cell lines (Emran et al .) and human melanoma tissues (TCGA) were assessed. Pearson correlation coefficient ( r ) and corresponding p values ( p )were presented.

Techniques: Cell Culture

(A) Differentially expressed genes (DEGs) between control and CRISPR-KO B16F10 were identified based on RNAseq analysis of bulk tumors, MACS-sorted tumor cells or cultured cells. Unique or common genes upregulated (upper) or downregulated (lower) were plotted in Venn diagrams. (B-C) Activated or repressed pathways (B) and upstream regulators (C) of identified DEGs were analyzed using Ingenuity Pathway Analysis (IPA). (D) Heatmaps show the Spearman correlation coefficient (upper) and corresponding p values (lower) in the comparison of expression of 15 genes commonly up- or down-regulated in RNAseq data from the three samples described in (A). X- and Y-axes indicate up/down-regulated genes and 10 IFNγ signature genes, respectively. CXCL10, FKBP10 and NACC1 were significantly correlated with NR2F6 and IFNγ signature. (E) Overall survival of melanoma patients with low or high expression of CXCL10, FKBP10 or NACC1 in melanoma specimens, as assessed by Kaplan-Meier analysis. Statistical significance was assessed by long-rank test.

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A) Differentially expressed genes (DEGs) between control and CRISPR-KO B16F10 were identified based on RNAseq analysis of bulk tumors, MACS-sorted tumor cells or cultured cells. Unique or common genes upregulated (upper) or downregulated (lower) were plotted in Venn diagrams. (B-C) Activated or repressed pathways (B) and upstream regulators (C) of identified DEGs were analyzed using Ingenuity Pathway Analysis (IPA). (D) Heatmaps show the Spearman correlation coefficient (upper) and corresponding p values (lower) in the comparison of expression of 15 genes commonly up- or down-regulated in RNAseq data from the three samples described in (A). X- and Y-axes indicate up/down-regulated genes and 10 IFNγ signature genes, respectively. CXCL10, FKBP10 and NACC1 were significantly correlated with NR2F6 and IFNγ signature. (E) Overall survival of melanoma patients with low or high expression of CXCL10, FKBP10 or NACC1 in melanoma specimens, as assessed by Kaplan-Meier analysis. Statistical significance was assessed by long-rank test.

Techniques: Control, CRISPR, Cell Culture, Comparison, Expressing

(A) B16F10 cells were transduced with scrambled [Scr (puromycin resistant), B-Scr (blasticidin resistant)] and two shRNAs (#334 for NACC1 KD and #876 for FKBP10 KD). mRNA and protein expression were assessed by qPCR and immunoblotting. (B) Growth of transduced cells in vitro was assessed using CellTiter-Glo. (C-D) The transduced cells were inoculated to C57BL/6 (C) or NSG (D) mice. Tumor growth was monitored at indicated time points. (E) B16F10 control cells (NR2F6 WT) or NR2F6 KO cells (#492 and #495) were inoculated to C57BL/6 control or NR2F6 KO mice. Tumor volumes were monitored at indicated time points. Data are presented as means ± SD. Statistical significance was assessed by student’s t-test (A, B, C, D), or two-way ANOVA with Tukey’s test (E).

Journal: bioRxiv

Article Title: Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

doi: 10.1101/2022.09.14.508028

Figure Lengend Snippet: (A) B16F10 cells were transduced with scrambled [Scr (puromycin resistant), B-Scr (blasticidin resistant)] and two shRNAs (#334 for NACC1 KD and #876 for FKBP10 KD). mRNA and protein expression were assessed by qPCR and immunoblotting. (B) Growth of transduced cells in vitro was assessed using CellTiter-Glo. (C-D) The transduced cells were inoculated to C57BL/6 (C) or NSG (D) mice. Tumor growth was monitored at indicated time points. (E) B16F10 control cells (NR2F6 WT) or NR2F6 KO cells (#492 and #495) were inoculated to C57BL/6 control or NR2F6 KO mice. Tumor volumes were monitored at indicated time points. Data are presented as means ± SD. Statistical significance was assessed by student’s t-test (A, B, C, D), or two-way ANOVA with Tukey’s test (E).

Techniques: Transduction, Expressing, Western Blot, In Vitro, Control

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