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A Comparison of <t>PHF10</t> IHC scores across various differentiation levels of GC ( n = 190). B A histogram illustration of PHF10 positivity in normal gastric mucosa, chronic gastritis, intestinal metaplasia and GC tissues. C Results from GO analysis. Genes of the epidermis development and epidermal cell differentiation were mostly enriched. D Results from KEGG enrichment analysis. Genes of the protein digestion, gastric acid secretion and IL-17 signaling pathway were enriched. E GSEA analysis revealed dysregulated pathways associated with PHF10 expression. The GSEA analysis of GO between the high and low PHF10 expression samples revealed significant difference in the enrichment of cell differentiation pathways, while the GSEA analysis of KEGG pathway enrichment showed MAPK signaling pathway activation. F WB validation of PHF10 knockdown SGC7901, PHF10 overexpression MKN28 and GES-1 cells. G QRT-PCR detection of gastric epithelial maturation and differentiation markers following PHF10 knockdown in SGC7901 cells. H The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in SGC7901-shPHF10 cells. I The expression patterns of markers for gastric epithelial maturation and differentiation following the upregulation of PHF10 in MKN28 cells. J The expression levels of CD44, CE133, Villin 1 and SOX9 in MKN28-PHF10 cells. K The expression of markers for gastric epithelial maturation and differentiation in GES-PHF10 cells. L The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in GES-1 cells overexpressing shPHF10. * P < 0.05.

Phf10, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phf10 - by Bioz Stars, 2026-03

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1) Product Images from "PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis"

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

Journal: Cancer Gene Therapy

doi: 10.1038/s41417-024-00820-5

A Comparison of PHF10 IHC scores across various differentiation levels of GC ( n = 190). B A histogram illustration of PHF10 positivity in normal gastric mucosa, chronic gastritis, intestinal metaplasia and GC tissues. C Results from GO analysis. Genes of the epidermis development and epidermal cell differentiation were mostly enriched. D Results from KEGG enrichment analysis. Genes of the protein digestion, gastric acid secretion and IL-17 signaling pathway were enriched. E GSEA analysis revealed dysregulated pathways associated with PHF10 expression. The GSEA analysis of GO between the high and low PHF10 expression samples revealed significant difference in the enrichment of cell differentiation pathways, while the GSEA analysis of KEGG pathway enrichment showed MAPK signaling pathway activation. F WB validation of PHF10 knockdown SGC7901, PHF10 overexpression MKN28 and GES-1 cells. G QRT-PCR detection of gastric epithelial maturation and differentiation markers following PHF10 knockdown in SGC7901 cells. H The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in SGC7901-shPHF10 cells. I The expression patterns of markers for gastric epithelial maturation and differentiation following the upregulation of PHF10 in MKN28 cells. J The expression levels of CD44, CE133, Villin 1 and SOX9 in MKN28-PHF10 cells. K The expression of markers for gastric epithelial maturation and differentiation in GES-PHF10 cells. L The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in GES-1 cells overexpressing shPHF10. * P < 0.05.

Figure Legend Snippet: A Comparison of PHF10 IHC scores across various differentiation levels of GC ( n = 190). B A histogram illustration of PHF10 positivity in normal gastric mucosa, chronic gastritis, intestinal metaplasia and GC tissues. C Results from GO analysis. Genes of the epidermis development and epidermal cell differentiation were mostly enriched. D Results from KEGG enrichment analysis. Genes of the protein digestion, gastric acid secretion and IL-17 signaling pathway were enriched. E GSEA analysis revealed dysregulated pathways associated with PHF10 expression. The GSEA analysis of GO between the high and low PHF10 expression samples revealed significant difference in the enrichment of cell differentiation pathways, while the GSEA analysis of KEGG pathway enrichment showed MAPK signaling pathway activation. F WB validation of PHF10 knockdown SGC7901, PHF10 overexpression MKN28 and GES-1 cells. G QRT-PCR detection of gastric epithelial maturation and differentiation markers following PHF10 knockdown in SGC7901 cells. H The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in SGC7901-shPHF10 cells. I The expression patterns of markers for gastric epithelial maturation and differentiation following the upregulation of PHF10 in MKN28 cells. J The expression levels of CD44, CE133, Villin 1 and SOX9 in MKN28-PHF10 cells. K The expression of markers for gastric epithelial maturation and differentiation in GES-PHF10 cells. L The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in GES-1 cells overexpressing shPHF10. * P < 0.05.

Techniques Used: Comparison, Cell Differentiation, Expressing, Activation Assay, Knockdown, Over Expression, Quantitative RT-PCR

A SGC7901 cells exhibited numerous microvilli on the cell surface and pits on the nuclear membrane (×15,000). B SGC7901 cells manifested a significant presence of rough endoplasmic reticulum in the cytoplasm (white arrow), limited mitochondrial cristae (black arrow) (×60,000). C SGC7901-shPHF10 cells exhibited a decrease in microvilli and pits on the nuclear membrane (×10,000). D SGC7901-shPHF10 cells presented a notable quantity of lysosomes with high electron density (white arrow) (×60,000). E The cytoplasm of SGC7901-shPHF10 cell exhibited an increase in mitochondrial cristae (white arrow) (×60,000). F Cells with PHF10 knockdown displayed alterations in the Golgi complex (white arrow) (×30,000). G Cytoplasmic vacuolization was observed in SGC7901-shPHF10 cells (×30,000). H Apoptotic cells were identified in SGC7901-shPHF10 cells (×15,000). I – K The sphere formation capacity of SGC-7901, MKN28 and GES-1 cells manipulated by PHF10 was evaluated by measuring the number and diameter of primary and secondary spheres separately. * P < 0.05; ** P < 0.01; *** P < 0.001.

Figure Legend Snippet: A SGC7901 cells exhibited numerous microvilli on the cell surface and pits on the nuclear membrane (×15,000). B SGC7901 cells manifested a significant presence of rough endoplasmic reticulum in the cytoplasm (white arrow), limited mitochondrial cristae (black arrow) (×60,000). C SGC7901-shPHF10 cells exhibited a decrease in microvilli and pits on the nuclear membrane (×10,000). D SGC7901-shPHF10 cells presented a notable quantity of lysosomes with high electron density (white arrow) (×60,000). E The cytoplasm of SGC7901-shPHF10 cell exhibited an increase in mitochondrial cristae (white arrow) (×60,000). F Cells with PHF10 knockdown displayed alterations in the Golgi complex (white arrow) (×30,000). G Cytoplasmic vacuolization was observed in SGC7901-shPHF10 cells (×30,000). H Apoptotic cells were identified in SGC7901-shPHF10 cells (×15,000). I – K The sphere formation capacity of SGC-7901, MKN28 and GES-1 cells manipulated by PHF10 was evaluated by measuring the number and diameter of primary and secondary spheres separately. * P < 0.05; ** P < 0.01; *** P < 0.001.

Techniques Used: Membrane, Knockdown

A The expression of differentiation markers in mice xenografts was compared between the SGC7901-shPHF10 and control groups. B The levels of various markers were assessed in the MKN28-PHF10 and control groups using qRT-PCR. C The morphology of xenografts in the SGC7901-NC and SGC7901-shPHF10 groups was examined through HE staining (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in the SGC7901-shPHF10 group exhibited a more organized arrangement and formed gastric gland tubular structures compared to those in the SGC7901-NC group. D The morphology of xenografts in the MKN28-vector and MKN28-PHF10 groups was examined (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in xenografts formed by MKN28-PHF10 and MKN28-vector exhibited diffuse and irregular distribution, lacking the formation of glandular-like structures. E – G IHC staining was performed on SGC7901-shPHF10 cells within the glandular tubular structure of SGC7901-shPHF10 xenografts (×200). Nuclei were represented in blue, ATP4B was represented in yellow in panel ( E ), PGC was represented in yellow in panel ( F ), and panel ( G ) showed negative expression of Adiponectin. H The expression level of E2F1 mRNA in normal and GC tissues. I The co-expression of E2F1 and PHF10 in GC tissue. J The analysis of PHF10 and E2F1 mRNA levels in SGC7901 cells following knockdown of E2F1 or PHF10. K The examination of PHF10 and E2F1 mRNA levels in MKN28 cells overexpressing E2F1 or PHF10. L The examination of PHF10 and E2F1 protein levels in SGC7901 cells after knockdown of E2F1 or PHF10. M The assessment of PHF10 and E2F1 protein levels in MKN28 cells following overexpression of E2F1 or PHF10. N , O ChIP-qPCR experiments in SGC7901 ( N ) and MKN28-E2F1 ( O ) cells. P Dual luciferase reporter assay in MKN28-E2F1 and MKN28-E2F1 vector cells. * P < 0.05; ** P < 0.01; *** P < 0.001.

Figure Legend Snippet: A The expression of differentiation markers in mice xenografts was compared between the SGC7901-shPHF10 and control groups. B The levels of various markers were assessed in the MKN28-PHF10 and control groups using qRT-PCR. C The morphology of xenografts in the SGC7901-NC and SGC7901-shPHF10 groups was examined through HE staining (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in the SGC7901-shPHF10 group exhibited a more organized arrangement and formed gastric gland tubular structures compared to those in the SGC7901-NC group. D The morphology of xenografts in the MKN28-vector and MKN28-PHF10 groups was examined (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in xenografts formed by MKN28-PHF10 and MKN28-vector exhibited diffuse and irregular distribution, lacking the formation of glandular-like structures. E – G IHC staining was performed on SGC7901-shPHF10 cells within the glandular tubular structure of SGC7901-shPHF10 xenografts (×200). Nuclei were represented in blue, ATP4B was represented in yellow in panel ( E ), PGC was represented in yellow in panel ( F ), and panel ( G ) showed negative expression of Adiponectin. H The expression level of E2F1 mRNA in normal and GC tissues. I The co-expression of E2F1 and PHF10 in GC tissue. J The analysis of PHF10 and E2F1 mRNA levels in SGC7901 cells following knockdown of E2F1 or PHF10. K The examination of PHF10 and E2F1 mRNA levels in MKN28 cells overexpressing E2F1 or PHF10. L The examination of PHF10 and E2F1 protein levels in SGC7901 cells after knockdown of E2F1 or PHF10. M The assessment of PHF10 and E2F1 protein levels in MKN28 cells following overexpression of E2F1 or PHF10. N , O ChIP-qPCR experiments in SGC7901 ( N ) and MKN28-E2F1 ( O ) cells. P Dual luciferase reporter assay in MKN28-E2F1 and MKN28-E2F1 vector cells. * P < 0.05; ** P < 0.01; *** P < 0.001.

Techniques Used: Expressing, Control, Quantitative RT-PCR, Staining, Plasmid Preparation, Immunohistochemistry, Knockdown, Over Expression, Luciferase, Reporter Assay

A , B The nuclear co-localization of PHF10 and BRG1 was observed in SGC7901 cells ( A ) and MKN28 cells ( B ). C – F Co-IP assays were performed using antibodies against PHF10 ( C ), BRG1 ( D ), BAF155 ( E ) and SNF5 ( F ) in SGC7901-shPHF10 and control cells. G – J Co-IP experiments for PHF10 ( G ), BRG1 ( H ), BAF155 ( I ) and SNF5 ( J ) were conducted in MKN28-PHF10 and control cells.

Figure Legend Snippet: A , B The nuclear co-localization of PHF10 and BRG1 was observed in SGC7901 cells ( A ) and MKN28 cells ( B ). C – F Co-IP assays were performed using antibodies against PHF10 ( C ), BRG1 ( D ), BAF155 ( E ) and SNF5 ( F ) in SGC7901-shPHF10 and control cells. G – J Co-IP experiments for PHF10 ( G ), BRG1 ( H ), BAF155 ( I ) and SNF5 ( J ) were conducted in MKN28-PHF10 and control cells.

Techniques Used: Co-Immunoprecipitation Assay, Control

A – C Detection of E2F1, PHF10 and DUSP5 expression in SGC7901 cells by qRT-PCR. D – F The mRNA levels of E2F1, PHF10 and DUSP5 in MKN28 cells were also assessed. G , H WB analysis was performed to determine the levels of DUSP5, ERK1/2 and pERK1/2 levels in SGC7901 cells. I The levels of E2F1, PHF10, DUSP5, ERK1/2 and pERK1/2 levels in MKN28 cells were evaluated. J ChIP-qPCR was carried out using antibodies against PHF10, BRG1, BAF155 and SNF5 in SGC7901 cells, with IgG antibodies serving as a negative control. The purified DNA after precipitation was subsequently amplified using the same set of primers for PCR analysis. K The promoter region of DUSP5 was amplified in MKN28-PHF10 cells using antibodies against PHF10, BRG1, BAF155 and SNF5. L A dual luciferase reporter assay was conducted in both MKN28-PHF10-Vector and MKN28-PHF10 cells.

Figure Legend Snippet: A – C Detection of E2F1, PHF10 and DUSP5 expression in SGC7901 cells by qRT-PCR. D – F The mRNA levels of E2F1, PHF10 and DUSP5 in MKN28 cells were also assessed. G , H WB analysis was performed to determine the levels of DUSP5, ERK1/2 and pERK1/2 levels in SGC7901 cells. I The levels of E2F1, PHF10, DUSP5, ERK1/2 and pERK1/2 levels in MKN28 cells were evaluated. J ChIP-qPCR was carried out using antibodies against PHF10, BRG1, BAF155 and SNF5 in SGC7901 cells, with IgG antibodies serving as a negative control. The purified DNA after precipitation was subsequently amplified using the same set of primers for PCR analysis. K The promoter region of DUSP5 was amplified in MKN28-PHF10 cells using antibodies against PHF10, BRG1, BAF155 and SNF5. L A dual luciferase reporter assay was conducted in both MKN28-PHF10-Vector and MKN28-PHF10 cells.

Techniques Used: Expressing, Quantitative RT-PCR, Negative Control, Purification, Amplification, Luciferase, Reporter Assay, Plasmid Preparation

A The relationship between E2F1 or PHF10 and DUSP5, was examined in 30 pairs of GC tissues through qRT-PCR analysis. B IHC staining was performed for E2F1, PHF10 and DUSP5 in two patient samples. Patient 1 exhibited poorly differentiated and diffuse GC, while patient 2 had well differentiated and intestinal GC. C WB analysis was conducted to measure the levels of E2F1, PHF10, DUSP5 and pERK1/2 in the aforementioned patient samples. D The expression levels of gastric epithelium differentiation markers (ATP4B, PG I, GAST, TFF1, CD44 and SOX9) were detected by qRT-PCR in SGC7901 cells. E The mRNA levels of gastric epithelium differentiation markers were assessed in MKN28 cells. F , G Sphere formation was quantified in SGC7901 cells ( F ) and MKN28 cells ( G ). H A schematic illustrating the mechanism of PHF10-mediated dysdifferentiation in GC cells.

Figure Legend Snippet: A The relationship between E2F1 or PHF10 and DUSP5, was examined in 30 pairs of GC tissues through qRT-PCR analysis. B IHC staining was performed for E2F1, PHF10 and DUSP5 in two patient samples. Patient 1 exhibited poorly differentiated and diffuse GC, while patient 2 had well differentiated and intestinal GC. C WB analysis was conducted to measure the levels of E2F1, PHF10, DUSP5 and pERK1/2 in the aforementioned patient samples. D The expression levels of gastric epithelium differentiation markers (ATP4B, PG I, GAST, TFF1, CD44 and SOX9) were detected by qRT-PCR in SGC7901 cells. E The mRNA levels of gastric epithelium differentiation markers were assessed in MKN28 cells. F , G Sphere formation was quantified in SGC7901 cells ( F ) and MKN28 cells ( G ). H A schematic illustrating the mechanism of PHF10-mediated dysdifferentiation in GC cells.

Techniques Used: Quantitative RT-PCR, Immunohistochemistry, Expressing

Image Search Results

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A Comparison of PHF10 IHC scores across various differentiation levels of GC ( n = 190). B A histogram illustration of PHF10 positivity in normal gastric mucosa, chronic gastritis, intestinal metaplasia and GC tissues. C Results from GO analysis. Genes of the epidermis development and epidermal cell differentiation were mostly enriched. D Results from KEGG enrichment analysis. Genes of the protein digestion, gastric acid secretion and IL-17 signaling pathway were enriched. E GSEA analysis revealed dysregulated pathways associated with PHF10 expression. The GSEA analysis of GO between the high and low PHF10 expression samples revealed significant difference in the enrichment of cell differentiation pathways, while the GSEA analysis of KEGG pathway enrichment showed MAPK signaling pathway activation. F WB validation of PHF10 knockdown SGC7901, PHF10 overexpression MKN28 and GES-1 cells. G QRT-PCR detection of gastric epithelial maturation and differentiation markers following PHF10 knockdown in SGC7901 cells. H The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in SGC7901-shPHF10 cells. I The expression patterns of markers for gastric epithelial maturation and differentiation following the upregulation of PHF10 in MKN28 cells. J The expression levels of CD44, CE133, Villin 1 and SOX9 in MKN28-PHF10 cells. K The expression of markers for gastric epithelial maturation and differentiation in GES-PHF10 cells. L The expression levels of gastric epithelial stem progenitor cells and GC stem cell markers in GES-1 cells overexpressing shPHF10. * P < 0.05.

Article Snippet: The following antibodies were used: PHF10 (Novus, USA, H00055274-D01), E2F1 (Santa Cruz, sc-193), BRG1 (Santa Cruz, sc-17796), SNF5 (Santa Cruz, sc-16189), BAF155 (Santa Cruz, sc-10756).

Techniques: Comparison, Cell Differentiation, Expressing, Activation Assay, Knockdown, Over Expression, Quantitative RT-PCR

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A SGC7901 cells exhibited numerous microvilli on the cell surface and pits on the nuclear membrane (×15,000). B SGC7901 cells manifested a significant presence of rough endoplasmic reticulum in the cytoplasm (white arrow), limited mitochondrial cristae (black arrow) (×60,000). C SGC7901-shPHF10 cells exhibited a decrease in microvilli and pits on the nuclear membrane (×10,000). D SGC7901-shPHF10 cells presented a notable quantity of lysosomes with high electron density (white arrow) (×60,000). E The cytoplasm of SGC7901-shPHF10 cell exhibited an increase in mitochondrial cristae (white arrow) (×60,000). F Cells with PHF10 knockdown displayed alterations in the Golgi complex (white arrow) (×30,000). G Cytoplasmic vacuolization was observed in SGC7901-shPHF10 cells (×30,000). H Apoptotic cells were identified in SGC7901-shPHF10 cells (×15,000). I – K The sphere formation capacity of SGC-7901, MKN28 and GES-1 cells manipulated by PHF10 was evaluated by measuring the number and diameter of primary and secondary spheres separately. * P < 0.05; ** P < 0.01; *** P < 0.001.

Techniques: Membrane, Knockdown

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A The expression of differentiation markers in mice xenografts was compared between the SGC7901-shPHF10 and control groups. B The levels of various markers were assessed in the MKN28-PHF10 and control groups using qRT-PCR. C The morphology of xenografts in the SGC7901-NC and SGC7901-shPHF10 groups was examined through HE staining (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in the SGC7901-shPHF10 group exhibited a more organized arrangement and formed gastric gland tubular structures compared to those in the SGC7901-NC group. D The morphology of xenografts in the MKN28-vector and MKN28-PHF10 groups was examined (×200, ×400). Nuclei were represented in blue, while cytoplasm was represented in red. Tumor cells in xenografts formed by MKN28-PHF10 and MKN28-vector exhibited diffuse and irregular distribution, lacking the formation of glandular-like structures. E – G IHC staining was performed on SGC7901-shPHF10 cells within the glandular tubular structure of SGC7901-shPHF10 xenografts (×200). Nuclei were represented in blue, ATP4B was represented in yellow in panel ( E ), PGC was represented in yellow in panel ( F ), and panel ( G ) showed negative expression of Adiponectin. H The expression level of E2F1 mRNA in normal and GC tissues. I The co-expression of E2F1 and PHF10 in GC tissue. J The analysis of PHF10 and E2F1 mRNA levels in SGC7901 cells following knockdown of E2F1 or PHF10. K The examination of PHF10 and E2F1 mRNA levels in MKN28 cells overexpressing E2F1 or PHF10. L The examination of PHF10 and E2F1 protein levels in SGC7901 cells after knockdown of E2F1 or PHF10. M The assessment of PHF10 and E2F1 protein levels in MKN28 cells following overexpression of E2F1 or PHF10. N , O ChIP-qPCR experiments in SGC7901 ( N ) and MKN28-E2F1 ( O ) cells. P Dual luciferase reporter assay in MKN28-E2F1 and MKN28-E2F1 vector cells. * P < 0.05; ** P < 0.01; *** P < 0.001.

Techniques: Expressing, Control, Quantitative RT-PCR, Staining, Plasmid Preparation, Immunohistochemistry, Knockdown, Over Expression, Luciferase, Reporter Assay

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A , B The nuclear co-localization of PHF10 and BRG1 was observed in SGC7901 cells ( A ) and MKN28 cells ( B ). C – F Co-IP assays were performed using antibodies against PHF10 ( C ), BRG1 ( D ), BAF155 ( E ) and SNF5 ( F ) in SGC7901-shPHF10 and control cells. G – J Co-IP experiments for PHF10 ( G ), BRG1 ( H ), BAF155 ( I ) and SNF5 ( J ) were conducted in MKN28-PHF10 and control cells.

Techniques: Co-Immunoprecipitation Assay, Control

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A – C Detection of E2F1, PHF10 and DUSP5 expression in SGC7901 cells by qRT-PCR. D – F The mRNA levels of E2F1, PHF10 and DUSP5 in MKN28 cells were also assessed. G , H WB analysis was performed to determine the levels of DUSP5, ERK1/2 and pERK1/2 levels in SGC7901 cells. I The levels of E2F1, PHF10, DUSP5, ERK1/2 and pERK1/2 levels in MKN28 cells were evaluated. J ChIP-qPCR was carried out using antibodies against PHF10, BRG1, BAF155 and SNF5 in SGC7901 cells, with IgG antibodies serving as a negative control. The purified DNA after precipitation was subsequently amplified using the same set of primers for PCR analysis. K The promoter region of DUSP5 was amplified in MKN28-PHF10 cells using antibodies against PHF10, BRG1, BAF155 and SNF5. L A dual luciferase reporter assay was conducted in both MKN28-PHF10-Vector and MKN28-PHF10 cells.

Techniques: Expressing, Quantitative RT-PCR, Negative Control, Purification, Amplification, Luciferase, Reporter Assay, Plasmid Preparation

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Figure Lengend Snippet: A The relationship between E2F1 or PHF10 and DUSP5, was examined in 30 pairs of GC tissues through qRT-PCR analysis. B IHC staining was performed for E2F1, PHF10 and DUSP5 in two patient samples. Patient 1 exhibited poorly differentiated and diffuse GC, while patient 2 had well differentiated and intestinal GC. C WB analysis was conducted to measure the levels of E2F1, PHF10, DUSP5 and pERK1/2 in the aforementioned patient samples. D The expression levels of gastric epithelium differentiation markers (ATP4B, PG I, GAST, TFF1, CD44 and SOX9) were detected by qRT-PCR in SGC7901 cells. E The mRNA levels of gastric epithelium differentiation markers were assessed in MKN28 cells. F , G Sphere formation was quantified in SGC7901 cells ( F ) and MKN28 cells ( G ). H A schematic illustrating the mechanism of PHF10-mediated dysdifferentiation in GC cells.

Techniques: Quantitative RT-PCR, Immunohistochemistry, Expressing

(A) Schematic of the modified FIRE-Cas9 system showing induced proximity by dimerization of Frb and Fkbp domains by rapamycin. (B) Lentiviral expression constructs of FIRE-Cas9 components. (C) Western blot showing expression of dCas9-HA and MS2-2xFrb in each cell line with WT TC1 negative and total protein staining controls. (D) Western blot showing expression of 2xFkbp-V5–tagged BAF subunits used to recruit their respective complexes with WT TC1 negative and total protein staining controls. (E) Co-IP pulldown with an antibody against V5 followed by Western blot showing interactions between V5-tagged BAF subunits and the core subunit BAF155 and the ATPase BRG1. (F) Co-IP pulldown with an antibody against V5 followed by Western blot in a WT cell line not expressing the V5 tag showing the lack of interactions between V5-tagged BAF subunits and the core subunit BAF155 and the ATPase BRG1. (G) Co-IP pulldown with an antibody against the pBAF-specific subunit ARID2 showing interactions with BRG1, BAF155, and PHF10-2xFkbp-V5. Source data are available for this figure.

Journal: Life Science Alliance

Article Title: Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes

doi: 10.26508/lsa.202402715

Figure Lengend Snippet: (A) Schematic of the modified FIRE-Cas9 system showing induced proximity by dimerization of Frb and Fkbp domains by rapamycin. (B) Lentiviral expression constructs of FIRE-Cas9 components. (C) Western blot showing expression of dCas9-HA and MS2-2xFrb in each cell line with WT TC1 negative and total protein staining controls. (D) Western blot showing expression of 2xFkbp-V5–tagged BAF subunits used to recruit their respective complexes with WT TC1 negative and total protein staining controls. (E) Co-IP pulldown with an antibody against V5 followed by Western blot showing interactions between V5-tagged BAF subunits and the core subunit BAF155 and the ATPase BRG1. (F) Co-IP pulldown with an antibody against V5 followed by Western blot in a WT cell line not expressing the V5 tag showing the lack of interactions between V5-tagged BAF subunits and the core subunit BAF155 and the ATPase BRG1. (G) Co-IP pulldown with an antibody against the pBAF-specific subunit ARID2 showing interactions with BRG1, BAF155, and PHF10-2xFkbp-V5. Source data are available for this figure.

Article Snippet: Protein G beads washed with PBS are incubated with each antibody, mouse ɑ-V5 Tag (E9H8O) (1:50; Cell Signaling Technology), rabbit ɑ-PHF10 (1:100; Invitrogen), and rabbit ɑ-ARID2 (1:100; Invitrogen) in PBS for 1 h at RT.

Techniques: Modification, Expressing, Construct, Western Blot, Staining, Co-Immunoprecipitation Assay

Chromatin immunoprecipitations followed by qPCR detecting enrichment of the unique recruited subunits. 0 bp denotes the TSS of Nkx2-9 and the recruitment site spans −172 to −25 bp (upstream of the TSS). Data are presented as bound/input either no recruitment (control) or recruitment (RAP). (A) Pulldown of DPF2-2xFkbp-V5 with an antibody against V5 (cBAF). (B) Pulldown of BRD9-2xFkbp-V5 with an antibody against V5 (gBAF). (C) Pulldown of PHF10-2xFkbp-V5 with an antibody against PHF10 (pBAF) (n = 5; mean ± s.e.m.). Significance was evaluated by multiple Mann-Whitney tests. * denotes q < 0.05.

Journal: Life Science Alliance

Article Title: Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes

doi: 10.26508/lsa.202402715

Figure Lengend Snippet: Chromatin immunoprecipitations followed by qPCR detecting enrichment of the unique recruited subunits. 0 bp denotes the TSS of Nkx2-9 and the recruitment site spans −172 to −25 bp (upstream of the TSS). Data are presented as bound/input either no recruitment (control) or recruitment (RAP). (A) Pulldown of DPF2-2xFkbp-V5 with an antibody against V5 (cBAF). (B) Pulldown of BRD9-2xFkbp-V5 with an antibody against V5 (gBAF). (C) Pulldown of PHF10-2xFkbp-V5 with an antibody against PHF10 (pBAF) (n = 5; mean ± s.e.m.). Significance was evaluated by multiple Mann-Whitney tests. * denotes q < 0.05.

Techniques: Control, MANN-WHITNEY

(A) Enrichment of V5 with cBAF versus gBAF under rapamycin-based recruitment conditions shows no statistical difference in recruitment enrichment. (B) . V5 enrichment with pBAF recruitment via PHF10-2xFkbp-V5 under control and rapamycin-based recruitment (RAP) conditions (C) . V5 versus PHF10 enrichment with pBAF recruitment via PHF10-2xFkbp-V5 after rapamycin addition. Data are presented as bound/input either no recruitment or recruitment (n = 4–5; mean ± s.e.m.).

Journal: Life Science Alliance

Article Title: Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes

doi: 10.26508/lsa.202402715

Figure Lengend Snippet: (A) Enrichment of V5 with cBAF versus gBAF under rapamycin-based recruitment conditions shows no statistical difference in recruitment enrichment. (B) . V5 enrichment with pBAF recruitment via PHF10-2xFkbp-V5 under control and rapamycin-based recruitment (RAP) conditions (C) . V5 versus PHF10 enrichment with pBAF recruitment via PHF10-2xFkbp-V5 after rapamycin addition. Data are presented as bound/input either no recruitment or recruitment (n = 4–5; mean ± s.e.m.).

Techniques: Control

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Article Snippet: IHC was conducted in adherence to established procedures, utilizing primary antibodies targeting PHF10 (GeneTex, GTX116314), E2F1 (Santa Cruz, sc-193), DUSP5 (Santa Cruz, sc-393801), ATP4B (Santa Cruz, sc-376393), PGC (Santa Cruz, sc-5815), and a biotinylated swine anti-rabbit secondary antibody (Dako, Denmark).

Techniques: Comparison, Cell Differentiation, Expressing, Activation Assay, Biomarker Discovery, Knockdown, Over Expression, Quantitative RT-PCR

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Membrane, Knockdown

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Expressing, Control, Quantitative RT-PCR, Staining, Plasmid Preparation, Immunohistochemistry, Knockdown, Over Expression, ChIP-qPCR, Luciferase, Reporter Assay

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Co-Immunoprecipitation Assay, Control

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Expressing, Quantitative RT-PCR, ChIP-qPCR, Negative Control, Purification, Amplification, Luciferase, Reporter Assay, Plasmid Preparation

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Quantitative RT-PCR, Immunohistochemistry, Expressing

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Article Snippet: The primary antibodies utilized in this study included PHF10 (GeneTex, USA, GTX116314), E2F1 (Santa Cruz, USA, sc-193), DUSP5 (Santa Cruz, sc-393801), BRG1 (Santa Cruz, sc-17796), SNF5 (Santa Cruz, sc-16189), BAF155 (Santa Cruz, sc-10756), BRM (Abcam, USA, ab15597), ERK1/2 (Cell Signaling, USA, CST9926), and pERK1/2 (Cell Signaling, CST9910).

Techniques: Comparison, Cell Differentiation, Expressing, Activation Assay, Biomarker Discovery, Knockdown, Over Expression, Quantitative RT-PCR

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Membrane, Knockdown

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Expressing, Control, Quantitative RT-PCR, Staining, Plasmid Preparation, Immunohistochemistry, Knockdown, Over Expression, ChIP-qPCR, Luciferase, Reporter Assay

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Co-Immunoprecipitation Assay, Control

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Expressing, Quantitative RT-PCR, ChIP-qPCR, Negative Control, Purification, Amplification, Luciferase, Reporter Assay, Plasmid Preparation

Journal: Cancer Gene Therapy

Article Title: PHF10 inhibits gastric epithelium differentiation and induces gastric cancer carcinogenesis

doi: 10.1038/s41417-024-00820-5

Techniques: Quantitative RT-PCR, Immunohistochemistry, Expressing

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