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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

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

Modification:

Article Title: Id2 Complexes with the SNAG Domain of Snai1 Inhibiting Snai1-Mediated Repression of Integrin β4
Article Snippet: .. NMuMG (normal murine mammary gland) cells were purchased from ATCC and maintained in complete medium containing Dulbecco’s modified Eagle’s medium (DMEM) (high glucose) with 10% fetal bovine serum, 10 g/ml insulin, 100 g/ml streptomycin, and 100 units/ml penicillin at 37°C in an incubator supplied with 5% CO2. .. Transforming growth factor (TGF- ; Peprotech) was added directly into the culture medium at a final concentration of 4 ng/ml for the time periods indicated in the figure legends.

Article Title: Id2 Complexes with the SNAG Domain of Snai1 Inhibiting Snai1-Mediated Repression of Integrin ?4
Article Snippet: .. NMuMG (normal murine mammary gland) cells were purchased from ATCC and maintained in complete medium containing Dulbecco's modified Eagle's medium (DMEM) (high glucose) with 10% fetal bovine serum, 10 μg/ml insulin, 100 μg/ml streptomycin, and 100 units/ml penicillin at 37°C in an incubator supplied with 5% CO 2 . .. Transforming growth factor β (TGF-β; Peprotech) was added directly into the culture medium at a final concentration of 4 ng/ml for the time periods indicated in the figure legends.

Article Title: The nucleus forms a dynamic contact with the plasma membrane to maintain the glandular epithelial architecture
Article Snippet: .. NMuMG (Normal Murine Mammary Gland) cells were from ATCC and were cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 1X penicillin-streptomycin mix (Pen-Strep), and 10 μg/ml insulin. .. MCF-10A human breast epithelial cells were obtained from ATCC and maintained as previously described ( ).

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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

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.

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

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.

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

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.

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

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.

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

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normal murine mammary gland nmumg epithelial cells (ATCC)

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