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Journal: Discover Oncology
Article Title: CENP-F promotes HCC cell proliferation mediated by super enhancer reader BRD4
doi: 10.1007/s12672-025-03785-5
Figure Lengend Snippet: Analysis of correlations with each other among CENP-F and related genes. (A) The PPI network for CENP-F, CDK1, CDK2, CDK7 and BRD4 in human species. (B) The PPI network for CENP-F, CDK1, CDK2, CDK7 and BRD4 in mouse species. (C) The correlation between CENP-F and CDK1 in HCC. (D) The correlation between BRD4 and CDK1 in HCC. (E) The correlation between CENP-F and CDK2 in HCC. (F) The correlation between BRD4 and CDK2 in HCC. (G) The correlation between CENP-F and BRD4 in HCC
Article Snippet: The
Techniques:
Journal: Discover Oncology
Article Title: CENP-F promotes HCC cell proliferation mediated by super enhancer reader BRD4
doi: 10.1007/s12672-025-03785-5
Figure Lengend Snippet: The mRNA expression of CENP-F and related genes in HCC. (A) The mRNA expression levels of CENP-F in HCC. (B) The mRNA expression levels of CDK1 in HCC. (C) The mRNA expression levels of CDK2 in HCC. (D) The mRNA expression levels of BRD4 in HCC. *<0.05, **<0.01, *** <0.001, ****<0.0001 vs. match control. Statistical significance was tested by Student’s t -test. Data represent mean ± SEM of more than three independent experiments
Article Snippet: The
Techniques: Expressing, Control
Journal: Discover Oncology
Article Title: CENP-F promotes HCC cell proliferation mediated by super enhancer reader BRD4
doi: 10.1007/s12672-025-03785-5
Figure Lengend Snippet: The expression of mRNA and protein levels of related genes after knockdown CENP-F and overexpression of CENP-F in vitro. (A) RT-qPCR analysis of CENP-F expression in HepG2 cell line among the normal contral (NC) group, shCENP-F group, empty vector group and overexpression group. (B) RT-qPCR analysis of CDK1 expression in HepG2 cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (C) RT-qPCR analysis of CDK2 expression in HepG2 cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (D) RT-qPCR analysis of BRD4 expression in HepG2 cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (E) RT-qPCR analysis of c-Myc expression in HepG2 cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (F) RT-qPCR analysis of CENP-F expression in Hep3B cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (G) RT-qPCR analysis of CDK1 expression in Hep3B cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (H) RT-qPCR analysis of CDK2 expression in Hep3B cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (I) RT-qPCR analysis of BRD4 expression in Hep3B cell line among the NC group, shCENP-F group, empty vector group and overexpression group. (J) RT-qPCR analysis of c-Myc expression in Hep3B cell line among the NC group, shCENP-F group, empty vector group and overexpression group. K. Western blotting analysis of CENP-F, CDK1, CDK2, BRD4 and c-Myc expression in HepG2 cell line. L. Western blotting analysis of CENP-F, CDK1, CDK2, BRD4 and c-Myc expression in Hep3B cell line. *<0.05, **<0.01, *** <0.001, ****<0.0001 vs. match control. Statistical significance was tested by Student’s t -test. Data represent mean ± SEM of three independent experiments
Article Snippet: The
Techniques: Expressing, Knockdown, Over Expression, In Vitro, Quantitative RT-PCR, Plasmid Preparation, Western Blot, Control
Journal: Discover Oncology
Article Title: CENP-F promotes HCC cell proliferation mediated by super enhancer reader BRD4
doi: 10.1007/s12672-025-03785-5
Figure Lengend Snippet: Knockdown CENP-F and BRD4 inhibited HCC cell proliferation in vivo. (A) Subcutaneous tumor model of HCC among NC group, shBRD4 and shCENP-F group. (B) Subcutaneous tumor size of HCC among NC group, shBRD4 and shCENP-F group. (C) Tumor growth volume comparison among NC group, shBRD4 and shCENP-F group. (D) Live imaging of tumor tissue after CENP-F inhibition. (E) Live imaging of tumor tissue after BRD4 inhibition. (F) RT-qPCR analysis of CENP-F expression in tumor tissue between the NC group and the shCENP-F group. (G) RT-qPCR analysis of CDK1 expression in tumor tissue between the NC group and the shCENP-F group. (H) RT-qPCR analysis of CDK2 expression in tumor tissue between the NC group and the shCENP-F group. (I) RT-qPCR analysis of BRD4 expression in tumor tissue between the NC group and the shCENP-F group. (J) RT-qPCR analysis of c-Myc expression in tumor tissue between the NC group and the shCENP-F group. K. RT-qPCR analysis of BRD4 expression in tumor tissue between the NC group and the shBRD4 group. L. RT-qPCR analysis of c-Myc expression in tumor tissue between the NC group and the shBRD4 group. M. Western blotting analysis of CENP-F, CDK1, CDK2, BRD4 and c-Myc expression in tumor tissue between the NC group and the shCENP-F group. N. Western blotting analysis of BRD4 and c-Myc expression in tumor tissue between the NC group and the shBRD4 group. *<0.05, **<0.01, *** <0.001, ****<0.0001 vs. match control. Statistical significance was tested by Student’s t -test. Data represent mean ± SEM of three or six independent experiments
Article Snippet: The
Techniques: Knockdown, In Vivo, Comparison, Imaging, Inhibition, Quantitative RT-PCR, Expressing, Western Blot, Control
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: TGF-β-induced BRD4 expression along with SMC markers in 10T1/2 cells. ( A , B ), TGF-β-induced BRD4 and SMC marker expression dose dependently in 10T1/2 cells. Serum-starved 10T1/2 cells were treated with vehicle or different concentrations of TGF-β as indicated for 48 h. BRD4 and VSMC markers (α-SMA and SM22α) were detected by Western blotting (WB, ( A )) and quantified in ( B ). Tubulin served as the loading control. *, p < 0.05 compared to vehicle group (0 ng/mL, ( B )), n = 3 independent experiments. ( C , D ), 10T1/2 cells were starved for 24 h, followed by vehicle or TGF-β (5 ng/mL) induction for various times as indicated. WB ( C ) and qPCR ( D ) were performed to detect BRD4 and SMC marker protein and mRNA expression, respectively. *, p < 0.05 compared to vehicle group (0 h, ( D )), n = 3 replicates. Cyclophilin was the internal control for qPCR.
Article Snippet: The small molecular inhibitor of
Techniques: Expressing, Marker, Western Blot, Control
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 knockdown attenuated TGF-β-induced differentiation of 10T1/2 cells to SMCs. ( A ), 10T1/2 cells were transfected with scramble or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 48 h. The expression of BRD4 and SMC markers was detected by WB ( A ). ( B ) is the quantification of A based on 3 independent experiments. *, p < 0.05 compared to vehicle-treated scramble; #, p < 0.05 compared to TGF-β-treated scramble.
Article Snippet: The small molecular inhibitor of
Techniques: Knockdown, Transfection, Expressing
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 inhibitor JQ1 inhibited TGF-β-induced differentiation of 10T1/2 cells into SMCs. ( A , B ), serum-starved 10T1/2 cells were pretreated with different doses of JQ1, followed by TGF-β treatment for an additional 48 h, and cells were then harvested for WB analysis of SMC markers. Tubulin was used as the loading control. B is the quantification of A based on 3 independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. ( C ), Serum-starved 10T1/2 cells were pretreated with different doses of JQ1, followed by TGF-β treatment for an additional 16 h before cells were harvested for qPCR analysis of SMC markers. Cyclophilin was used as an internal control. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. n = 3 replicates.
Article Snippet: The small molecular inhibitor of
Techniques: Control
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 degraders inhibited TGF-β-induced differentiation of 10T1/2 cells into SMCs. ( A , C ), Serum-starved 10T1/2 cells were pretreated with different doses of ARV-825 (ARV, ( A )) or dBET1 ( C ), followed by TGF-β treatment (5 ng/mL) for an additional 48 h, and the cells were then harvested for WB analysis of SMC markers. Tubulin was used as the loading control. ( B , D ) are the quantification of ( A , C ), respectively, based on 3 independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group.
Article Snippet: The small molecular inhibitor of
Techniques: Control
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 knockdown inhibited TGF-β-induced TAZ expression in 10T1/2 cells. ( A , B ), Serum-starved 10T1/2 cells were treated with TGF-β treatment (5 ng/mL) for different times as indicated before the cells were harvested for WB ( A ) and qPCR ( B ) analysis of TAZ. Tubulin was used as the loading control. Cyclophilin was used as the internal control for qPCR analysis in B. *, p < 0.05 compared to control (0 h), n = 3 replicates. ( C ), 10T1/2 cells were transfected with scramble control or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 8 h. The cells were then harvested for analysis of given protein by WB. ( D ) is the quantification of C based on 3 independent experiments. *, p < 0.05 compared to the vehicle-treated scramble; #, p < 0.05 compared to TGF-β-treated scramble.
Article Snippet: The small molecular inhibitor of
Techniques: Knockdown, Expressing, Control, Transfection
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 inhibitors suppressed TGF-β-induced TAZ expression in 10T1/2 cells. ( A ), serum-starved 10T1/2 cells were pretreated with JQ1 (2 µM), dBET1 (100 nM), or ARV-825 (ARV, 100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 8 h. The cells were then harvested for WB analysis of TAZ. Tubulin was used as the loading control. ( B ) is the quantification of A based on 3 independent experiments. *, p < 0.05 compared with vehicle control; #, p < 0.05 compared to TGF-β treatment alone group. ( C – E ), serum-starved 10T1/2 cells were pretreated with different doses of JQ1 ( C ), ARV-825 (ARV, ( D )) or dBET1 ( E ), followed by TGF-β treatment (5 ng/mL) for an additional 8 h to detect TAZ through WB.
Article Snippet: The small molecular inhibitor of
Techniques: Expressing, Control
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: Myocardin is involved in BRD4 mediated10T1/2 differentiation into SMCs. ( A ) Serum-starved 10T1/2 cells were treated with TGF-β (5 ng/mL) for various times to detect Myocardin expression through WB. ( B ) is the quantification of A based on three independent experiments. *, p < 0.05 compared with control (0 h). ( C ) 10T1/2 cells were transfected with scramble control or siBRD4, followed by treatment with vehicle or TGF-β (5 ng/mL) for an additional 24 h. Myocardin expression was detected through WB. ( D ) is the quantification of C based on three independent experiments. *, p < 0.05 compared with the vehicle-treated scramble; #, p < 0.05 compared with TGF-β-treated scramble. ( E ) serum-starved 10T1/2 cells were pretreated with JQ1 (2 µM), dBET1 (100 nM), or ARV-825 (100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 24 h. The cells were then harvested for WB analysis of myocardin. ( F ) is the quantification of E based on three independent experiments. *, p < 0.05 compared to vehicle control; #, p < 0.05 compared to TGF-β treatment alone group.
Article Snippet: The small molecular inhibitor of
Techniques: Expressing, Control, Transfection
Journal: International Journal of Molecular Sciences
Article Title: BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells
doi: 10.3390/ijms26168074
Figure Lengend Snippet: BRD4 inhibition reduced the nuclear levels of Smad3 induced by TGF-β in 10T1/2 cells. ( A ) Serum-starved 10T1/2 cells were pretreated with ARV-825 (100 nM) for 30 min, followed by TGF-β treatment (5 ng/mL) for an additional 2 h, and cells were then subject to immunofluorescence staining of Smad3. Images were taken at 200×. ( B ) Serum-starved 10T1/2 cells were pretreated with JQ1 (1 µM) or ARV-825 (100 nM), followed by TGF-β treatment (5 ng/mL) for an additional 2 h, and cells were then subject to fractionation WB analysis of Smad3. Tubulin and Lamin B1 were used as loading controls for the cytoplasm and nucleus, respectively.
Article Snippet: The small molecular inhibitor of
Techniques: Inhibition, Immunofluorescence, Staining, Fractionation
Journal: Communications biology
Article Title: USP35 promotes the growth of ER positive breast cancer by inhibiting ferroptosis via BRD4-SLC7A11 axis.
doi: 10.1038/s42003-025-07513-1
Figure Lengend Snippet: Fig. 8 | A working model of USP35 regulating ferroptosis in ER+ breast cancer tumors. USP35 interacts with and deubiquitinates BRD4, stabilizing the protein level of BRD4 that regulates SLC7A11. This interaction leads to USP35-invoked upregu- lating SLC7A11 expression, inhibiting ferroptosis, and promoting cell growth in ER+ breast cancer.
Article Snippet: Breast cancer cells MCF-7 (8000 per well) and ZR-75-1 (12,000 per well) were cultured in 24-well tissue culture plates and treated with DMSO or 5 μM (+ )-
Techniques: Expressing