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normal murine mammary gland nmumg epithelial cells  (ATCC)


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    ATCC normal murine mammary gland nmumg epithelial cells
    Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in <t>NMuMG</t> cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.
    Normal Murine Mammary Gland Nmumg Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 572 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade"

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    Journal: FASEB BioAdvances

    doi: 10.1096/fba.2025-00117

    Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in NMuMG cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in NMuMG cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Immunofluorescence, Staining, Cell Culture, Control, Western Blot, Quantitative Proteomics

    Inhibition of G9a activity impacts H3K9 dimethylation levels and EMT in response to TGFβ1 and matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA for NMuMG cells cultured on hydrogels and treated with DMSO or the G9a inhibitor UNC0642 (10 nM) with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of αSMA positive NMuMG cells for various treatment conditions from immunofluorescence staining for αSMA. Data represent mean ± sem for n = 4 independent experiments, ** p < 0.01, *** p < 0.001. (D) Western blots for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells. Densitometric quantification of the relative expression of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from western blots shown in panel (D). Data are normalized with respect to the soft hydrogel DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Figure Legend Snippet: Inhibition of G9a activity impacts H3K9 dimethylation levels and EMT in response to TGFβ1 and matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA for NMuMG cells cultured on hydrogels and treated with DMSO or the G9a inhibitor UNC0642 (10 nM) with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of αSMA positive NMuMG cells for various treatment conditions from immunofluorescence staining for αSMA. Data represent mean ± sem for n = 4 independent experiments, ** p < 0.01, *** p < 0.001. (D) Western blots for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells. Densitometric quantification of the relative expression of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from western blots shown in panel (D). Data are normalized with respect to the soft hydrogel DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Techniques Used: Inhibition, Activity Assay, Immunofluorescence, Staining, Cell Culture, Western Blot, Expressing, Control

    siRNA knockdown of G9a attenuates TGFβ1‐induced changes in H3K9me2, αSMA, and N‐cadherin levels as a function of matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of the percentage of αSMA positive cells for various treatment conditions. Data represent mean ± sem for n = 4 independent experiments, *** p < 0.001. (D) Western blot for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Densitometric quantification of the relative levels of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from blots shown in panel (D). Data are normalized with respect to the soft NTC siRNA control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Figure Legend Snippet: siRNA knockdown of G9a attenuates TGFβ1‐induced changes in H3K9me2, αSMA, and N‐cadherin levels as a function of matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of the percentage of αSMA positive cells for various treatment conditions. Data represent mean ± sem for n = 4 independent experiments, *** p < 0.001. (D) Western blot for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Densitometric quantification of the relative levels of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from blots shown in panel (D). Data are normalized with respect to the soft NTC siRNA control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Techniques Used: Knockdown, Immunofluorescence, Staining, Transfection, Western Blot, Control

    Knockdown of G9a impacts YAP subcellular localization and inhibiting YAP attenuates TGFβ1‐induced αSMA expression and cell morphology changes as a function of matrix stiffness. (A) Immunofluorescence staining for YAP in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (B) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization under different treatment conditions. Data represent mean ± sem for n = 3; # p < 0.001 with respect to all other samples, * p < 0.05 with respect to the stiff hydrogel siG9a control and soft hydrogel siG9a TGFβ1 samples. (C) Immunofluorescence staining for αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or YAP inhibitor Verteporfin (4 μM) with and without TGFβ1 treatment. Scale bars: 25 μm. (D) Quantification of αSMA positive NMuMG cells cultured on soft and stiff hydrogels and treated with DMSO or Verteporfin in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; *** p < 0.001.
    Figure Legend Snippet: Knockdown of G9a impacts YAP subcellular localization and inhibiting YAP attenuates TGFβ1‐induced αSMA expression and cell morphology changes as a function of matrix stiffness. (A) Immunofluorescence staining for YAP in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (B) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization under different treatment conditions. Data represent mean ± sem for n = 3; # p < 0.001 with respect to all other samples, * p < 0.05 with respect to the stiff hydrogel siG9a control and soft hydrogel siG9a TGFβ1 samples. (C) Immunofluorescence staining for αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or YAP inhibitor Verteporfin (4 μM) with and without TGFβ1 treatment. Scale bars: 25 μm. (D) Quantification of αSMA positive NMuMG cells cultured on soft and stiff hydrogels and treated with DMSO or Verteporfin in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; *** p < 0.001.

    Techniques Used: Knockdown, Expressing, Immunofluorescence, Staining, Transfection, Control, Cell Culture

    G9a regulates LATS kinase which acts upstream of YAP and αSMA. (A) Quantitative real‐time PCR for LATS2 and (B) relative levels of LATS2 quantified from immunofluorescence staining in NMuMG cells cultured on hydrogels with storage moduli of 260 Pa and 2200 Pa and transfected with non‐targeting control siRNA (NTC) or siRNA targeting G9a (siG9a#2) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization in cells following treatment with DMSO or LATS1/2 kinase inhibitor TRULI (15 μM) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01 with respect to soft DMSO control sample, # p < 0.01 with respect to stiff DMSO control sample, a p < 0.001 with respect to all other samples except stiff TRULI TGFβ1, b p < 0.001 with respect to all other samples. Immunofluorescence staining for (D) YAP and (E) αSMA in NMuMG cells under different treatment conditions. Scale bars: 25 μm. (F) Quantification of αSMA positive NMuMG cells treated with DMSO or TRULI in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; ** p < 0.01, *** p < 0.001. (G) Western blot for E‐cadherin and αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or TRULI with and without treatment with TGFβ1. Densitometric quantification of the relative expression of (H) E‐cadherin and (I) αSMA from western blots shown in panel (G). Data are normalized with respect to the soft DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: G9a regulates LATS kinase which acts upstream of YAP and αSMA. (A) Quantitative real‐time PCR for LATS2 and (B) relative levels of LATS2 quantified from immunofluorescence staining in NMuMG cells cultured on hydrogels with storage moduli of 260 Pa and 2200 Pa and transfected with non‐targeting control siRNA (NTC) or siRNA targeting G9a (siG9a#2) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization in cells following treatment with DMSO or LATS1/2 kinase inhibitor TRULI (15 μM) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01 with respect to soft DMSO control sample, # p < 0.01 with respect to stiff DMSO control sample, a p < 0.001 with respect to all other samples except stiff TRULI TGFβ1, b p < 0.001 with respect to all other samples. Immunofluorescence staining for (D) YAP and (E) αSMA in NMuMG cells under different treatment conditions. Scale bars: 25 μm. (F) Quantification of αSMA positive NMuMG cells treated with DMSO or TRULI in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; ** p < 0.01, *** p < 0.001. (G) Western blot for E‐cadherin and αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or TRULI with and without treatment with TGFβ1. Densitometric quantification of the relative expression of (H) E‐cadherin and (I) αSMA from western blots shown in panel (G). Data are normalized with respect to the soft DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Cell Culture, Transfection, Control, Western Blot, Expressing

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    Modification:

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    Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in <t>NMuMG</t> cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.
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    Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in NMuMG cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: FASEB BioAdvances

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    doi: 10.1096/fba.2025-00117

    Figure Lengend Snippet: Matrix stiffness regulates G9a and histone 3 lysine 9 dimethylation in response to TGFβ1. Immunofluorescence staining for (A) G9a and (B) H3K9me2 in NMuMG cells cultured on hydrogels and treated with or without TGFβ1. Scale bars: 25 μm. Quantification of the (C) relative nuclear G9a and (D) relative H3K9me2 levels from immunofluorescence images shown in panels (A) and (B). Data are normalized with respect to the soft hydrogel control sample. (E) Western blot for G9a using whole cell protein extracts and H3K9me2 using histone extracts from NMuMG cells cultured on hydrogels with and without TGFβ1 treatment. Relative quantification via densitometric analysis for (F) G9a and (G) H3K9me2 from blots shown in panel (E). Data are normalized with respect to the soft hydrogel control sample. All data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were obtained from American Type Culture Collection (ATCC Cat# CRL‐1636, RRID: CVCL_0075) and were maintained in Dulbecco's Modified Eagle Medium (DMEM; Corning) with 10% (v/v) fetal bovine serum (FBS; Atlanta Biologicals), 50 μg/mL gentamicin (Gibco), and 10 μg/mL insulin (Sigma Aldrich).

    Techniques: Immunofluorescence, Staining, Cell Culture, Control, Western Blot, Quantitative Proteomics

    Inhibition of G9a activity impacts H3K9 dimethylation levels and EMT in response to TGFβ1 and matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA for NMuMG cells cultured on hydrogels and treated with DMSO or the G9a inhibitor UNC0642 (10 nM) with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of αSMA positive NMuMG cells for various treatment conditions from immunofluorescence staining for αSMA. Data represent mean ± sem for n = 4 independent experiments, ** p < 0.01, *** p < 0.001. (D) Western blots for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells. Densitometric quantification of the relative expression of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from western blots shown in panel (D). Data are normalized with respect to the soft hydrogel DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: FASEB BioAdvances

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    doi: 10.1096/fba.2025-00117

    Figure Lengend Snippet: Inhibition of G9a activity impacts H3K9 dimethylation levels and EMT in response to TGFβ1 and matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA for NMuMG cells cultured on hydrogels and treated with DMSO or the G9a inhibitor UNC0642 (10 nM) with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of αSMA positive NMuMG cells for various treatment conditions from immunofluorescence staining for αSMA. Data represent mean ± sem for n = 4 independent experiments, ** p < 0.01, *** p < 0.001. (D) Western blots for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells. Densitometric quantification of the relative expression of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from western blots shown in panel (D). Data are normalized with respect to the soft hydrogel DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were obtained from American Type Culture Collection (ATCC Cat# CRL‐1636, RRID: CVCL_0075) and were maintained in Dulbecco's Modified Eagle Medium (DMEM; Corning) with 10% (v/v) fetal bovine serum (FBS; Atlanta Biologicals), 50 μg/mL gentamicin (Gibco), and 10 μg/mL insulin (Sigma Aldrich).

    Techniques: Inhibition, Activity Assay, Immunofluorescence, Staining, Cell Culture, Western Blot, Expressing, Control

    siRNA knockdown of G9a attenuates TGFβ1‐induced changes in H3K9me2, αSMA, and N‐cadherin levels as a function of matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of the percentage of αSMA positive cells for various treatment conditions. Data represent mean ± sem for n = 4 independent experiments, *** p < 0.001. (D) Western blot for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Densitometric quantification of the relative levels of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from blots shown in panel (D). Data are normalized with respect to the soft NTC siRNA control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: FASEB BioAdvances

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    doi: 10.1096/fba.2025-00117

    Figure Lengend Snippet: siRNA knockdown of G9a attenuates TGFβ1‐induced changes in H3K9me2, αSMA, and N‐cadherin levels as a function of matrix stiffness. Immunofluorescence staining for (A) E‐cadherin and (B) αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (C) Quantification of the percentage of αSMA positive cells for various treatment conditions. Data represent mean ± sem for n = 4 independent experiments, *** p < 0.001. (D) Western blot for H3K9me2, G9a, E‐cadherin, N‐cadherin, and αSMA in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Densitometric quantification of the relative levels of (E) H3K9me2, (F) G9a, (G) E‐cadherin, (H) αSMA, and (I) N‐cadherin from blots shown in panel (D). Data are normalized with respect to the soft NTC siRNA control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were obtained from American Type Culture Collection (ATCC Cat# CRL‐1636, RRID: CVCL_0075) and were maintained in Dulbecco's Modified Eagle Medium (DMEM; Corning) with 10% (v/v) fetal bovine serum (FBS; Atlanta Biologicals), 50 μg/mL gentamicin (Gibco), and 10 μg/mL insulin (Sigma Aldrich).

    Techniques: Knockdown, Immunofluorescence, Staining, Transfection, Western Blot, Control

    Knockdown of G9a impacts YAP subcellular localization and inhibiting YAP attenuates TGFβ1‐induced αSMA expression and cell morphology changes as a function of matrix stiffness. (A) Immunofluorescence staining for YAP in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (B) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization under different treatment conditions. Data represent mean ± sem for n = 3; # p < 0.001 with respect to all other samples, * p < 0.05 with respect to the stiff hydrogel siG9a control and soft hydrogel siG9a TGFβ1 samples. (C) Immunofluorescence staining for αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or YAP inhibitor Verteporfin (4 μM) with and without TGFβ1 treatment. Scale bars: 25 μm. (D) Quantification of αSMA positive NMuMG cells cultured on soft and stiff hydrogels and treated with DMSO or Verteporfin in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; *** p < 0.001.

    Journal: FASEB BioAdvances

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    doi: 10.1096/fba.2025-00117

    Figure Lengend Snippet: Knockdown of G9a impacts YAP subcellular localization and inhibiting YAP attenuates TGFβ1‐induced αSMA expression and cell morphology changes as a function of matrix stiffness. (A) Immunofluorescence staining for YAP in NMuMG cells transfected with NTC siRNA or siG9a#2 with and without TGFβ1 treatment. Scale bars: 25 μm. (B) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization under different treatment conditions. Data represent mean ± sem for n = 3; # p < 0.001 with respect to all other samples, * p < 0.05 with respect to the stiff hydrogel siG9a control and soft hydrogel siG9a TGFβ1 samples. (C) Immunofluorescence staining for αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or YAP inhibitor Verteporfin (4 μM) with and without TGFβ1 treatment. Scale bars: 25 μm. (D) Quantification of αSMA positive NMuMG cells cultured on soft and stiff hydrogels and treated with DMSO or Verteporfin in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; *** p < 0.001.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were obtained from American Type Culture Collection (ATCC Cat# CRL‐1636, RRID: CVCL_0075) and were maintained in Dulbecco's Modified Eagle Medium (DMEM; Corning) with 10% (v/v) fetal bovine serum (FBS; Atlanta Biologicals), 50 μg/mL gentamicin (Gibco), and 10 μg/mL insulin (Sigma Aldrich).

    Techniques: Knockdown, Expressing, Immunofluorescence, Staining, Transfection, Control, Cell Culture

    G9a regulates LATS kinase which acts upstream of YAP and αSMA. (A) Quantitative real‐time PCR for LATS2 and (B) relative levels of LATS2 quantified from immunofluorescence staining in NMuMG cells cultured on hydrogels with storage moduli of 260 Pa and 2200 Pa and transfected with non‐targeting control siRNA (NTC) or siRNA targeting G9a (siG9a#2) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization in cells following treatment with DMSO or LATS1/2 kinase inhibitor TRULI (15 μM) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01 with respect to soft DMSO control sample, # p < 0.01 with respect to stiff DMSO control sample, a p < 0.001 with respect to all other samples except stiff TRULI TGFβ1, b p < 0.001 with respect to all other samples. Immunofluorescence staining for (D) YAP and (E) αSMA in NMuMG cells under different treatment conditions. Scale bars: 25 μm. (F) Quantification of αSMA positive NMuMG cells treated with DMSO or TRULI in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; ** p < 0.01, *** p < 0.001. (G) Western blot for E‐cadherin and αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or TRULI with and without treatment with TGFβ1. Densitometric quantification of the relative expression of (H) E‐cadherin and (I) αSMA from western blots shown in panel (G). Data are normalized with respect to the soft DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: FASEB BioAdvances

    Article Title: Matrix Stiffness Regulates TGFβ1 ‐Induced αSMA Expression via a G9a‐ LATS ‐ YAP Signaling Cascade

    doi: 10.1096/fba.2025-00117

    Figure Lengend Snippet: G9a regulates LATS kinase which acts upstream of YAP and αSMA. (A) Quantitative real‐time PCR for LATS2 and (B) relative levels of LATS2 quantified from immunofluorescence staining in NMuMG cells cultured on hydrogels with storage moduli of 260 Pa and 2200 Pa and transfected with non‐targeting control siRNA (NTC) or siRNA targeting G9a (siG9a#2) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Quantification of the percentage of cells with nuclear (N), pancellular (N/C), or cytoplasmic (C) YAP localization in cells following treatment with DMSO or LATS1/2 kinase inhibitor TRULI (15 μM) with and without TGFβ1 treatment. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01 with respect to soft DMSO control sample, # p < 0.01 with respect to stiff DMSO control sample, a p < 0.001 with respect to all other samples except stiff TRULI TGFβ1, b p < 0.001 with respect to all other samples. Immunofluorescence staining for (D) YAP and (E) αSMA in NMuMG cells under different treatment conditions. Scale bars: 25 μm. (F) Quantification of αSMA positive NMuMG cells treated with DMSO or TRULI in the presence and absence of TGFβ1. Data represent mean ± sem for n = 3 independent experiments; ** p < 0.01, *** p < 0.001. (G) Western blot for E‐cadherin and αSMA in NMuMG cells cultured on hydrogels and treated with DMSO or TRULI with and without treatment with TGFβ1. Densitometric quantification of the relative expression of (H) E‐cadherin and (I) αSMA from western blots shown in panel (G). Data are normalized with respect to the soft DMSO control sample. Data represent mean ± sem for n = 3 independent experiments; * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were obtained from American Type Culture Collection (ATCC Cat# CRL‐1636, RRID: CVCL_0075) and were maintained in Dulbecco's Modified Eagle Medium (DMEM; Corning) with 10% (v/v) fetal bovine serum (FBS; Atlanta Biologicals), 50 μg/mL gentamicin (Gibco), and 10 μg/mL insulin (Sigma Aldrich).

    Techniques: Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Cell Culture, Transfection, Control, Western Blot, Expressing

    FIGURE 2 | Functional silencing of DSE2 attenuates Snail expression in A549 and NMuMG cells. (A) Design of guide RNAs targeting SNAI1 DSE1 and DSE2. (B, D) Immunoblot analysis of A549 or NMuMG cells with silenced DSEs. Protein expression was monitored after 3 h of TGF-β stim- ulation using the indicated antibodies. α-tubulin was used as a loading control. (C, E) Expression profiles of the indicated genes in A549 or NMuMG cells analyzed by qRT-PCR (triplicate determinations). Cells were stimulated with TGF-β for 1.5 h. Data are expressed as fold-change compared with unstimulated parental groups to show changes in basal expression. Statistical analysis was performed using Tukey's multiple comparison test (p > 0.05, n.s.; p < 0.001, ***).

    Journal: Cancer science

    Article Title: Identification of a Distal Enhancer That Regulates TGF-β-Induced SNAI1 Expression.

    doi: 10.1111/cas.70091

    Figure Lengend Snippet: FIGURE 2 | Functional silencing of DSE2 attenuates Snail expression in A549 and NMuMG cells. (A) Design of guide RNAs targeting SNAI1 DSE1 and DSE2. (B, D) Immunoblot analysis of A549 or NMuMG cells with silenced DSEs. Protein expression was monitored after 3 h of TGF-β stim- ulation using the indicated antibodies. α-tubulin was used as a loading control. (C, E) Expression profiles of the indicated genes in A549 or NMuMG cells analyzed by qRT-PCR (triplicate determinations). Cells were stimulated with TGF-β for 1.5 h. Data are expressed as fold-change compared with unstimulated parental groups to show changes in basal expression. Statistical analysis was performed using Tukey's multiple comparison test (p > 0.05, n.s.; p < 0.001, ***).

    Article Snippet: HepG2/C3A and normal murine mammary gland epithelial (NMuMG) cells were obtained from the American Type Culture Collection.

    Techniques: Functional Assay, Expressing, Western Blot, Control, Quantitative RT-PCR, Comparison

    Comparison of Saa1 and Saa3 mRNA expression levels in NMuMG cells treated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Data are presented as the mean ± standard deviation of four independent experiments. Asterisks indicate significant difference compared with control levels: ** p < 0.01. NMuMG, normal murine mammary gland.

    Journal: Animals : an Open Access Journal from MDPI

    Article Title: Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid

    doi: 10.3390/ani11061548

    Figure Lengend Snippet: Comparison of Saa1 and Saa3 mRNA expression levels in NMuMG cells treated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Data are presented as the mean ± standard deviation of four independent experiments. Asterisks indicate significant difference compared with control levels: ** p < 0.01. NMuMG, normal murine mammary gland.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were purchased from the European Collection of Authenticated Cell Cultures General Cell Collection, Public Health England (94081121, Salisbury, UK).

    Techniques: Comparison, Expressing, Standard Deviation, Control

    Comparison of SAA1 (A and B) and SAA3 (C and D) protein expression levels in NMuMG cells treated with lipopolysaccharide (LPS) or lipoteichoic acid (LTA) by immunofluorescence analysis (IFA). ( A , C ) Fields of view where fluorescence intensity was measured. Scale bar = 20 µm. ( B , D ) The relative SAA1 and SAA3 protein expression levels in NMuMG cells following stimulation with LPS or LTA were normalized to those in untreated, control cells. Data are presented as the mean fluorescence of five or more random locations with vertical bars representing standard deviation. Asterisks indicate significant difference compared with control levels: * p < 0.05, ** p < 0.01. NMuMG, normal murine mammary gland.

    Journal: Animals : an Open Access Journal from MDPI

    Article Title: Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid

    doi: 10.3390/ani11061548

    Figure Lengend Snippet: Comparison of SAA1 (A and B) and SAA3 (C and D) protein expression levels in NMuMG cells treated with lipopolysaccharide (LPS) or lipoteichoic acid (LTA) by immunofluorescence analysis (IFA). ( A , C ) Fields of view where fluorescence intensity was measured. Scale bar = 20 µm. ( B , D ) The relative SAA1 and SAA3 protein expression levels in NMuMG cells following stimulation with LPS or LTA were normalized to those in untreated, control cells. Data are presented as the mean fluorescence of five or more random locations with vertical bars representing standard deviation. Asterisks indicate significant difference compared with control levels: * p < 0.05, ** p < 0.01. NMuMG, normal murine mammary gland.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were purchased from the European Collection of Authenticated Cell Cultures General Cell Collection, Public Health England (94081121, Salisbury, UK).

    Techniques: Comparison, Expressing, Immunofluorescence, Fluorescence, Control, Standard Deviation

    Detection of SAA1 and SAA3 protein expression in NMuMG cell supernatants treated with lipopolysaccharide (LPS) or lipoteichoic acid (LTA) by Western blot. ( A ) Detection of SAA1 in the cell supernatant. Membranes were incubated with the primary anti-mouse SAA1 antibody (dilution of 1:500, 60 s exposure time). ( B ) Detection of SAA3 in the cell supernatant. Membranes were incubated with the primary anti-mouse SAA3 antibody (dilution of 1:50, 120 s exposure time). PC, positive control; 1, recombinant murine SAA1 (rSAA1); 3, rSAA3; NMuMG, normal murine mammary gland.

    Journal: Animals : an Open Access Journal from MDPI

    Article Title: Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid

    doi: 10.3390/ani11061548

    Figure Lengend Snippet: Detection of SAA1 and SAA3 protein expression in NMuMG cell supernatants treated with lipopolysaccharide (LPS) or lipoteichoic acid (LTA) by Western blot. ( A ) Detection of SAA1 in the cell supernatant. Membranes were incubated with the primary anti-mouse SAA1 antibody (dilution of 1:500, 60 s exposure time). ( B ) Detection of SAA3 in the cell supernatant. Membranes were incubated with the primary anti-mouse SAA3 antibody (dilution of 1:50, 120 s exposure time). PC, positive control; 1, recombinant murine SAA1 (rSAA1); 3, rSAA3; NMuMG, normal murine mammary gland.

    Article Snippet: Normal murine mammary gland (NMuMG) epithelial cells were purchased from the European Collection of Authenticated Cell Cultures General Cell Collection, Public Health England (94081121, Salisbury, UK).

    Techniques: Expressing, Western Blot, Incubation, Positive Control, Recombinant