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ERBB2 (HER2) was the top inhibited upstream regulator in noninvasive fibroblasts. (A) Flow cytometry analysis confirmed the overexpression of SEMA7A in lung fibroblasts. (B) Cell proliferation rates of fibroblasts with SEMA7A overexpression or control fibroblasts were determined by EdU assays. (C) Cell-surface expression of SEMA7A was determined by flow cytometry on single-cell homogenate of CD31 − , CD45 − , EPCAM − cells from IPF and healthy samples. (D) Single-cell Western blot confirmed the downregulation of <t>FOXF1</t> in invasive fibroblasts. (E and F) Dot plot visualization of the −Log 10 (FDR) (E) and bar plot visualization of the Activation Z-score (F) of the top 30 activated and inhibited upstream regulators of noninvasive fibroblasts by IPA analysis. ERBB2 was the top inhibited regulators of noninvasive fibroblasts. ERBB2 was highlighted as the most inhibited regulator. (G) The regulating network of invasive fibroblasts combining canonical signaling pathways and upstream regulators showed that the core signaling pathway was the invasion of tumor cell lines, suggesting that invasive lung fibroblasts had metastatic cancer-related signatures.
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ERBB2 (HER2) was the top inhibited upstream regulator in noninvasive fibroblasts. (A) Flow cytometry analysis confirmed the overexpression of SEMA7A in lung fibroblasts. (B) Cell proliferation rates of fibroblasts with SEMA7A overexpression or control fibroblasts were determined by EdU assays. (C) Cell-surface expression of SEMA7A was determined by flow cytometry on single-cell homogenate of CD31 − , CD45 − , EPCAM − cells from IPF and healthy samples. (D) Single-cell Western blot confirmed the downregulation of FOXF1 in invasive fibroblasts. (E and F) Dot plot visualization of the −Log 10 (FDR) (E) and bar plot visualization of the Activation Z-score (F) of the top 30 activated and inhibited upstream regulators of noninvasive fibroblasts by IPA analysis. ERBB2 was the top inhibited regulators of noninvasive fibroblasts. ERBB2 was highlighted as the most inhibited regulator. (G) The regulating network of invasive fibroblasts combining canonical signaling pathways and upstream regulators showed that the core signaling pathway was the invasion of tumor cell lines, suggesting that invasive lung fibroblasts had metastatic cancer-related signatures.

Journal: The Journal of Experimental Medicine

Article Title: HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts

doi: 10.1084/jem.20220126

Figure Lengend Snippet: ERBB2 (HER2) was the top inhibited upstream regulator in noninvasive fibroblasts. (A) Flow cytometry analysis confirmed the overexpression of SEMA7A in lung fibroblasts. (B) Cell proliferation rates of fibroblasts with SEMA7A overexpression or control fibroblasts were determined by EdU assays. (C) Cell-surface expression of SEMA7A was determined by flow cytometry on single-cell homogenate of CD31 − , CD45 − , EPCAM − cells from IPF and healthy samples. (D) Single-cell Western blot confirmed the downregulation of FOXF1 in invasive fibroblasts. (E and F) Dot plot visualization of the −Log 10 (FDR) (E) and bar plot visualization of the Activation Z-score (F) of the top 30 activated and inhibited upstream regulators of noninvasive fibroblasts by IPA analysis. ERBB2 was the top inhibited regulators of noninvasive fibroblasts. ERBB2 was highlighted as the most inhibited regulator. (G) The regulating network of invasive fibroblasts combining canonical signaling pathways and upstream regulators showed that the core signaling pathway was the invasion of tumor cell lines, suggesting that invasive lung fibroblasts had metastatic cancer-related signatures.

Article Snippet: Commercial siRNA used were listed: si- FOXF1 (sc-60655; Santa Cruz Biotechnology), si- CREBRF (sc-91839; Santa Cruz Biotechnology), si- TSC22D1 (16708; Thermo Fisher Scientific), si- MXI1 (sc-35835; Santa Cruz Biotechnology), si- KLF9 (sc-37716; Santa Cruz Biotechnology), si- NFE2L2 (sc-37030; Santa Cruz Biotechnology), si- HMGA2 (sc-37994; Santa Cruz Biotechnology) si- DPF3 (sc-92150; Santa Cruz Biotechnology).

Techniques: Flow Cytometry, Over Expression, Control, Expressing, Single Cell Western, Activation Assay, Protein-Protein interactions

Transcription factors regulated lung fibroblast invasion. (A–D) Knockdown of transcriptional factors was confirmed by qRT-PCR (A and B) and Western blotting (C and D). A, n = 9 for FOXF1 , n = 4 for CREBRF , TSC22D1, and KLF9 , n = 6 for MXI1 , n = 3 for NFE2L2 ; B, n = 4 for HMGA2 , n = 5 for DPF3 . (E) FOXF1 and SEMA7A expressions showed negative correlation in scRNA-seq by SeqGeq. (F and G) Relative mRNA levels of FOXF1 , SEMA7A , and collagen-related protein gene, ACTA2 and COL1A1 (F, n = 5 per group) and cell-surface expression of SEMA7A (G) after FOXF1 knockdown. (H–J) Representative images (H) and index quantification (I and J) of migration and invasion of fibroblasts after knockdown assay. I, FOXF1, CREBRF, TSC22D1, and MXI1, n = 6 for migration and invasion, KLF9, n = 3 for migration and invasion, NFE2L2, n = 3 for migration and n = 11 for invasion; J, HMGA2, n = 6 for migration and invasion, DPF3, n = 3 for migration and invasion. CTL, control; non, noninvasive; in, invasive. Three or four independent experiments were performed on fibroblasts from different patients (A, B, F, I, and J). Data are the mean ± SEM. Scale bar: 1 mm. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by Student’s t test. Source data are available for this figure: .

Journal: The Journal of Experimental Medicine

Article Title: HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts

doi: 10.1084/jem.20220126

Figure Lengend Snippet: Transcription factors regulated lung fibroblast invasion. (A–D) Knockdown of transcriptional factors was confirmed by qRT-PCR (A and B) and Western blotting (C and D). A, n = 9 for FOXF1 , n = 4 for CREBRF , TSC22D1, and KLF9 , n = 6 for MXI1 , n = 3 for NFE2L2 ; B, n = 4 for HMGA2 , n = 5 for DPF3 . (E) FOXF1 and SEMA7A expressions showed negative correlation in scRNA-seq by SeqGeq. (F and G) Relative mRNA levels of FOXF1 , SEMA7A , and collagen-related protein gene, ACTA2 and COL1A1 (F, n = 5 per group) and cell-surface expression of SEMA7A (G) after FOXF1 knockdown. (H–J) Representative images (H) and index quantification (I and J) of migration and invasion of fibroblasts after knockdown assay. I, FOXF1, CREBRF, TSC22D1, and MXI1, n = 6 for migration and invasion, KLF9, n = 3 for migration and invasion, NFE2L2, n = 3 for migration and n = 11 for invasion; J, HMGA2, n = 6 for migration and invasion, DPF3, n = 3 for migration and invasion. CTL, control; non, noninvasive; in, invasive. Three or four independent experiments were performed on fibroblasts from different patients (A, B, F, I, and J). Data are the mean ± SEM. Scale bar: 1 mm. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by Student’s t test. Source data are available for this figure: .

Article Snippet: Commercial siRNA used were listed: si- FOXF1 (sc-60655; Santa Cruz Biotechnology), si- CREBRF (sc-91839; Santa Cruz Biotechnology), si- TSC22D1 (16708; Thermo Fisher Scientific), si- MXI1 (sc-35835; Santa Cruz Biotechnology), si- KLF9 (sc-37716; Santa Cruz Biotechnology), si- NFE2L2 (sc-37030; Santa Cruz Biotechnology), si- HMGA2 (sc-37994; Santa Cruz Biotechnology) si- DPF3 (sc-92150; Santa Cruz Biotechnology).

Techniques: Knockdown, Quantitative RT-PCR, Western Blot, Expressing, Migration, Control

HER2 signaling activation increased fibroblast invasion and fibrosis. (A) The expression of invasive and noninvasive specific genes in HER2 overexpression normal fibroblasts were detected by qRT-PCR ( n = 3 per group). (B) Heatmap of the differentially expressed genes of control and HER2 overexpressing normal human lung fibroblasts by bulk RNA-seq. (C) Volcano plot of the top differentially expressed genes between control and HER2 overexpressed normal human lung fibroblasts by bulk RNA-seq. Red dots indicated the genes at Fold_change >0.5 and black dots indicated the genes at Fold_change ≤0.5. (D) Relative expression of invasive and noninvasive specific genes in HER2 overexpression normal fibroblasts detected by bulk RNA-seq ( n = 5 per group). (E) Upregulated cell-surface expression of SEMA7A in HER2 overexpression normal lung fibroblasts was confirmed by flow cytometry analysis. (F and G) Western blotting confirmation of the expression of p-HER2, HER2, SEMA7A, and FOXF1 in HER2 overexpression normal human lung fibroblasts (F) and quantification of the densitometry (G; n = 3 per group). GAPDH served as loading control. (H and I) Representative images (H) and index quantification (I; n = 6 per group) of normal lung fibroblast invasion after HER2 overexpression. (J and K) Trichrome staining (J) and hydroxyproline (K; n = 10 per group) of mice lungs receiving HER2 overexpressing and control normal human lung fibroblasts, and age-matched mice were treated with culture medium only. Dash-boxed regions were shown at higher magnification. CTL, control; OE, overexpression. Scale bar: 1 mm (H) and 500 μm (J). Three or four independent experiments were performed on fibroblasts from different patients (A, D, G, I, and K). Data are the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by Student’s t test (A, D, G, and I) and two-way ANOVA (K). Source data are available for this figure: .

Journal: The Journal of Experimental Medicine

Article Title: HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts

doi: 10.1084/jem.20220126

Figure Lengend Snippet: HER2 signaling activation increased fibroblast invasion and fibrosis. (A) The expression of invasive and noninvasive specific genes in HER2 overexpression normal fibroblasts were detected by qRT-PCR ( n = 3 per group). (B) Heatmap of the differentially expressed genes of control and HER2 overexpressing normal human lung fibroblasts by bulk RNA-seq. (C) Volcano plot of the top differentially expressed genes between control and HER2 overexpressed normal human lung fibroblasts by bulk RNA-seq. Red dots indicated the genes at Fold_change >0.5 and black dots indicated the genes at Fold_change ≤0.5. (D) Relative expression of invasive and noninvasive specific genes in HER2 overexpression normal fibroblasts detected by bulk RNA-seq ( n = 5 per group). (E) Upregulated cell-surface expression of SEMA7A in HER2 overexpression normal lung fibroblasts was confirmed by flow cytometry analysis. (F and G) Western blotting confirmation of the expression of p-HER2, HER2, SEMA7A, and FOXF1 in HER2 overexpression normal human lung fibroblasts (F) and quantification of the densitometry (G; n = 3 per group). GAPDH served as loading control. (H and I) Representative images (H) and index quantification (I; n = 6 per group) of normal lung fibroblast invasion after HER2 overexpression. (J and K) Trichrome staining (J) and hydroxyproline (K; n = 10 per group) of mice lungs receiving HER2 overexpressing and control normal human lung fibroblasts, and age-matched mice were treated with culture medium only. Dash-boxed regions were shown at higher magnification. CTL, control; OE, overexpression. Scale bar: 1 mm (H) and 500 μm (J). Three or four independent experiments were performed on fibroblasts from different patients (A, D, G, I, and K). Data are the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by Student’s t test (A, D, G, and I) and two-way ANOVA (K). Source data are available for this figure: .

Article Snippet: Commercial siRNA used were listed: si- FOXF1 (sc-60655; Santa Cruz Biotechnology), si- CREBRF (sc-91839; Santa Cruz Biotechnology), si- TSC22D1 (16708; Thermo Fisher Scientific), si- MXI1 (sc-35835; Santa Cruz Biotechnology), si- KLF9 (sc-37716; Santa Cruz Biotechnology), si- NFE2L2 (sc-37030; Santa Cruz Biotechnology), si- HMGA2 (sc-37994; Santa Cruz Biotechnology) si- DPF3 (sc-92150; Santa Cruz Biotechnology).

Techniques: Activation Assay, Expressing, Over Expression, Quantitative RT-PCR, Control, RNA Sequencing, Flow Cytometry, Western Blot, Staining

HER2 deficiency rescued the dysregulated gene profiles in IPF lung fibroblasts. (A–C) HER2 knockdown efficiency was confirmed by qRT-PCR (A) and Western blotting (B and C; A, n = 8 per group; C, n = 5 per group). (D) Cell-surface protein level of HER2 and SEMA7A in HER2 knockdown IPF lung fibroblasts. (E and F) Representative images (E) and index quantification (F; n = 9 per group) of fibroblast invasion after HER2 knockdown. (G) Protein levels of p-HER2, total HER2, SEMA7A, and FOXF1 in IPF lung fibroblasts after treatment of HER2 inhibitor, Lapatinib, at increasing concentrations. (H) Downregulation of cell-surface expression of SEMA7A, F3, and ITGA6 in Lapatinib-treated fibroblasts was determined by flow cytometry analysis. (I) Transcription levels of other representative genes in IPF lung fibroblasts after Lapatinib treatment were determined by qRT-PCR ( n = 3 per group). Scale bar: 1 mm (E). CTL, control; KD, knockdown. Three or four independent experiments were performed on fibroblasts from different patients (A, C, F, and I). Data are the mean ± SEM. *, P < 0.05; **, P < 0.01; ****, P < 0.0001 by Student’s t test (A, C, and F) or one-way ANOVA (I). Source data are available for this figure: .

Journal: The Journal of Experimental Medicine

Article Title: HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts

doi: 10.1084/jem.20220126

Figure Lengend Snippet: HER2 deficiency rescued the dysregulated gene profiles in IPF lung fibroblasts. (A–C) HER2 knockdown efficiency was confirmed by qRT-PCR (A) and Western blotting (B and C; A, n = 8 per group; C, n = 5 per group). (D) Cell-surface protein level of HER2 and SEMA7A in HER2 knockdown IPF lung fibroblasts. (E and F) Representative images (E) and index quantification (F; n = 9 per group) of fibroblast invasion after HER2 knockdown. (G) Protein levels of p-HER2, total HER2, SEMA7A, and FOXF1 in IPF lung fibroblasts after treatment of HER2 inhibitor, Lapatinib, at increasing concentrations. (H) Downregulation of cell-surface expression of SEMA7A, F3, and ITGA6 in Lapatinib-treated fibroblasts was determined by flow cytometry analysis. (I) Transcription levels of other representative genes in IPF lung fibroblasts after Lapatinib treatment were determined by qRT-PCR ( n = 3 per group). Scale bar: 1 mm (E). CTL, control; KD, knockdown. Three or four independent experiments were performed on fibroblasts from different patients (A, C, F, and I). Data are the mean ± SEM. *, P < 0.05; **, P < 0.01; ****, P < 0.0001 by Student’s t test (A, C, and F) or one-way ANOVA (I). Source data are available for this figure: .

Article Snippet: Commercial siRNA used were listed: si- FOXF1 (sc-60655; Santa Cruz Biotechnology), si- CREBRF (sc-91839; Santa Cruz Biotechnology), si- TSC22D1 (16708; Thermo Fisher Scientific), si- MXI1 (sc-35835; Santa Cruz Biotechnology), si- KLF9 (sc-37716; Santa Cruz Biotechnology), si- NFE2L2 (sc-37030; Santa Cruz Biotechnology), si- HMGA2 (sc-37994; Santa Cruz Biotechnology) si- DPF3 (sc-92150; Santa Cruz Biotechnology).

Techniques: Knockdown, Quantitative RT-PCR, Western Blot, Expressing, Flow Cytometry, Control