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hic1 (Bioss)

Name: hic1
Brand: Bioss
Rating: 92 (3 reviews)

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Bioss hic1
Hic1, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hic1/product/Bioss
Average 92 stars, based on 3 article reviews

hic1 - by Bioz Stars, 2026-02

92/100 stars

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(A) Representative whole-mount staining of the fourth inguinal mammary glands at the indicated ages (4 months and 8 months) were prepared from Hic1+/+ mice or Hic1–/– mice and stained with carmine aluminum (n = 6 for each group). M, months. (B) H&E staining of the mammary glands of 6-month-old mice. (C) Immunofluorescence staining of luminal epithelial marker (K8) and myoepithelial markers (α-SMA) in the mammary glands of 6-month-old, 8-month-old, and 12-month-old mice. (D) Immunohistochemical staining of Ki67 and cyclin D1 in mammary glands of 6-month-old mice. The dot plots show the mean value for each immunoreactivity score (IRS) with statistical evaluation. Data are shown as mean ± SEM. n = 6. *P < 0.05, 2-tailed Student’s t test. (E) Box plots of HIC1 mRNA levels in paired normal breast/BrCa tissues (left, paired t tests), non-TNBC/TNBC tissues (middle, 2-tailed Student’s t tests), and BrCa tissues at different stages (right, 1-way ANOVA followed by Bonferroni’s post hoc test). Data were obtained from the TCGA data set (TCGA_BRCA_exp_HiSeqV2-2015-02-24). *P < 0.05; **P < 0.01; ***P < 0.001. (F) Kaplan-Meier plots of the relapse-free survival of patients with BrCa in whole data sets stratified by HIC1 expression. Data were acquired from the Kaplan-Meier plotter database. P = 0.00027, log-rank test (28). Representative images in this figure were obtained from at least 3 animals of each genotype.

Journal: The Journal of Clinical Investigation

Article Title: HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk

doi: 10.1172/JCI99974

Figure Lengend Snippet: (A) Representative whole-mount staining of the fourth inguinal mammary glands at the indicated ages (4 months and 8 months) were prepared from Hic1+/+ mice or Hic1–/– mice and stained with carmine aluminum (n = 6 for each group). M, months. (B) H&E staining of the mammary glands of 6-month-old mice. (C) Immunofluorescence staining of luminal epithelial marker (K8) and myoepithelial markers (α-SMA) in the mammary glands of 6-month-old, 8-month-old, and 12-month-old mice. (D) Immunohistochemical staining of Ki67 and cyclin D1 in mammary glands of 6-month-old mice. The dot plots show the mean value for each immunoreactivity score (IRS) with statistical evaluation. Data are shown as mean ± SEM. n = 6. *P < 0.05, 2-tailed Student’s t test. (E) Box plots of HIC1 mRNA levels in paired normal breast/BrCa tissues (left, paired t tests), non-TNBC/TNBC tissues (middle, 2-tailed Student’s t tests), and BrCa tissues at different stages (right, 1-way ANOVA followed by Bonferroni’s post hoc test). Data were obtained from the TCGA data set (TCGA_BRCA_exp_HiSeqV2-2015-02-24). *P < 0.05; **P < 0.01; ***P < 0.001. (F) Kaplan-Meier plots of the relapse-free survival of patients with BrCa in whole data sets stratified by HIC1 expression. Data were acquired from the Kaplan-Meier plotter database. P = 0.00027, log-rank test (28). Representative images in this figure were obtained from at least 3 animals of each genotype.

Article Snippet: High-density TMA of human BrCa clinical samples (catalog BRC2281) were obtained from a cohort of 228 patients and constructed by Superbiotek Inc. IHC staining was performed with specific antibodies against HIC1 (catalog bs15485R; Bioss), CXCL14 (catalog ab46010; Abcam), CCL17 (catalog ab195044; Abcam), GPR85 (catalog ab140783; Abcam), and CCR4 (catalog ab1669; Abcam).

Techniques: Staining, Immunofluorescence, Marker, Immunohistochemical staining, Expressing

(A) Representative 3 immunohistochemistry images for α-SMA in mammary glands of 6-month-old mice. Positive staining in the mammary gland stroma of Hic1–/– mice is indicated by red arrows (n = 3 for each group). (B) CRISPR-Cas9–mediated HIC1 deletion in MCF7 and T47D luminal BrCa cells. Cell lysates were analyzed by Western blot with antibodies against HIC1 and GAPDH. sg3 and sg4 represent 2 different interference sgRNA sequences. Ctrl, control. (C) Representative primary NAFs and CAFs isolated from human BrCa tissues. Western blot analysis of cell lysates was performed using antibodies against α-SMA, FAP, PDGFRα, and GAPDH. (D) Schematic showing primary NAFs cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells in a Transwell apparatus (0.4 μm pore size) for 4 days. (E) Western blot analysis of lysates of NAF6 cells that were cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells for 4 days. Antibodies against α-SMA, FAP, PDGFRα, and GAPDH were used. (F) Immunofluorescence staining for the detection of α-SMA expression in NAF6 cells that were cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells for 4 days.

Journal: The Journal of Clinical Investigation

Article Title: HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk

doi: 10.1172/JCI99974

Figure Lengend Snippet: (A) Representative 3 immunohistochemistry images for α-SMA in mammary glands of 6-month-old mice. Positive staining in the mammary gland stroma of Hic1–/– mice is indicated by red arrows (n = 3 for each group). (B) CRISPR-Cas9–mediated HIC1 deletion in MCF7 and T47D luminal BrCa cells. Cell lysates were analyzed by Western blot with antibodies against HIC1 and GAPDH. sg3 and sg4 represent 2 different interference sgRNA sequences. Ctrl, control. (C) Representative primary NAFs and CAFs isolated from human BrCa tissues. Western blot analysis of cell lysates was performed using antibodies against α-SMA, FAP, PDGFRα, and GAPDH. (D) Schematic showing primary NAFs cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells in a Transwell apparatus (0.4 μm pore size) for 4 days. (E) Western blot analysis of lysates of NAF6 cells that were cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells for 4 days. Antibodies against α-SMA, FAP, PDGFRα, and GAPDH were used. (F) Immunofluorescence staining for the detection of α-SMA expression in NAF6 cells that were cocultured with MCF7CtrlMCF7sgHIC1 or T47DCtrlT47DsgHIC1 luminal BrCa cells for 4 days.

Techniques: Immunohistochemistry, Staining, CRISPR, Western Blot, Isolation, Immunofluorescence, Expressing

(A) Left: relative RT-qPCR analysis of 8 differentially expressed genes (CCL2, CXCL14, CX3CL1, IL1B, IL24, IL8, TGFA, and VEGFA) after HIC1 deletion in MCF7 and T47D cells (n = 3). Right: relative RT-qPCR analysis of Hic1, Cxcl14, and Sirt1 mRNA levels in the mammary glands of Hic1–/– or Hic1+/+ mice (n = 5). (B) ELISA analysis of CXCL14 levels in the CM of MCF7sgHIC1MCF7Ctrl and T47DsgHIC1T47DCtrl cells. The supernatants were collected after culture of the cells for 24 hours or 48 hours (n = 4). (C) Schematic of the CXCL14 promoter region. The positions of selected consensus binding sites are indicated above the diagram; the lengths of the promoter constructs used in the reporter assays are shown below. (D) CXCL14 promoter activity after transfection of the full-length construct (–2000/+136) alone or together with HIC1 expression vectors. p–GL3-Basic, control for promoter constructs; pc3.1, control for the HIC1 expression vector. The results are expressed as the ratio of firefly luciferase to Renilla luciferase (n = 3). (E) CXCL14 promoter activity after cotransfection with 100 ng of the HIC1 expression vector and each of the promoter constructs. The –41/+136 construct had a significant repressive effect, despite its lower promoter activity (n = 3). (F) ChIP analysis of HIC1 at the CXCL14 promoter region in MCF7 and T47D cells (n = 3). Data are shown as mean ± SEM. n = 3 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001, 2-tailed Student’s t tests (A, B, and E), 1-way ANOVA followed by Bonferroni’s post hoc test (D and F).

Journal: The Journal of Clinical Investigation

Article Title: HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk

doi: 10.1172/JCI99974

Figure Lengend Snippet: (A) Left: relative RT-qPCR analysis of 8 differentially expressed genes (CCL2, CXCL14, CX3CL1, IL1B, IL24, IL8, TGFA, and VEGFA) after HIC1 deletion in MCF7 and T47D cells (n = 3). Right: relative RT-qPCR analysis of Hic1, Cxcl14, and Sirt1 mRNA levels in the mammary glands of Hic1–/– or Hic1+/+ mice (n = 5). (B) ELISA analysis of CXCL14 levels in the CM of MCF7sgHIC1MCF7Ctrl and T47DsgHIC1T47DCtrl cells. The supernatants were collected after culture of the cells for 24 hours or 48 hours (n = 4). (C) Schematic of the CXCL14 promoter region. The positions of selected consensus binding sites are indicated above the diagram; the lengths of the promoter constructs used in the reporter assays are shown below. (D) CXCL14 promoter activity after transfection of the full-length construct (–2000/+136) alone or together with HIC1 expression vectors. p–GL3-Basic, control for promoter constructs; pc3.1, control for the HIC1 expression vector. The results are expressed as the ratio of firefly luciferase to Renilla luciferase (n = 3). (E) CXCL14 promoter activity after cotransfection with 100 ng of the HIC1 expression vector and each of the promoter constructs. The –41/+136 construct had a significant repressive effect, despite its lower promoter activity (n = 3). (F) ChIP analysis of HIC1 at the CXCL14 promoter region in MCF7 and T47D cells (n = 3). Data are shown as mean ± SEM. n = 3 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001, 2-tailed Student’s t tests (A, B, and E), 1-way ANOVA followed by Bonferroni’s post hoc test (D and F).

Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Binding Assay, Construct, Activity Assay, Transfection, Expressing, Plasmid Preparation, Luciferase, Cotransfection

(A) Percentages of low and high expression of epithelial HIC1 (upper), stromal CXCL14 (middle), and stromal CCL17 (bottom) in benign breast tissue and various BrCa subtypes are shown as a pie chart. P vs. benign, χ2 test. (B) Representative IHC images showing the correlation between epithelial HIC1 expression and stromal CXCL14/CCL17 expression in 228 benign and malignant breast tumor samples. Broken lines indicate the margins of the tumor. (C) Schematic model showing how HIC1-mediated crosstalk between cancer cells and mammary fibroblasts promotes BrCa progression. Conditional deletion of HIC1 in the mouse mammary gland may contribute to premalignant transformation at the early stage of breast tumor formation. Moreover, chemokine CXCL14 secreted by HIC1-deleted BrCa cells binds to its cognate receptor GPR85 on mammary fibroblasts in the microenvironment, thereby activating the fibroblasts through the ERK1/2, Akt, and neddylation pathways. The activated fibroblasts in turn promote BrCa progression through induction of EMT by activation of the CCL17/CCR4 chemokine axis.

Journal: The Journal of Clinical Investigation

Article Title: HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk

doi: 10.1172/JCI99974

Figure Lengend Snippet: (A) Percentages of low and high expression of epithelial HIC1 (upper), stromal CXCL14 (middle), and stromal CCL17 (bottom) in benign breast tissue and various BrCa subtypes are shown as a pie chart. P vs. benign, χ2 test. (B) Representative IHC images showing the correlation between epithelial HIC1 expression and stromal CXCL14/CCL17 expression in 228 benign and malignant breast tumor samples. Broken lines indicate the margins of the tumor. (C) Schematic model showing how HIC1-mediated crosstalk between cancer cells and mammary fibroblasts promotes BrCa progression. Conditional deletion of HIC1 in the mouse mammary gland may contribute to premalignant transformation at the early stage of breast tumor formation. Moreover, chemokine CXCL14 secreted by HIC1-deleted BrCa cells binds to its cognate receptor GPR85 on mammary fibroblasts in the microenvironment, thereby activating the fibroblasts through the ERK1/2, Akt, and neddylation pathways. The activated fibroblasts in turn promote BrCa progression through induction of EMT by activation of the CCL17/CCR4 chemokine axis.

Techniques: Expressing, Transformation Assay, Activation Assay

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