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antibodies against onecut2  (Bioss)


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    Structured Review

    Bioss antibodies against onecut2
    Antibodies Against Onecut2, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibodies+against+onecut2/ONECUT2+Polyclonal+Antibody/pm34253241-114-1-17
    Average 92 stars, based on 2 article reviews
    antibodies against onecut2 - by Bioz Stars, 2026-10
    92/100 stars

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    Related Articles

    Binding Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Luciferase:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Reporter Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Transfection:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Quantitative RT-PCR:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Western Blot:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Expressing:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Over Expression:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Plasmid Preparation:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Migration:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    EdU Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Colony Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Wound Healing Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Transwell Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Tube Formation Assay:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    In Vivo:

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway.
    Article Snippet: assay was performed as previously reported [24]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.

    Article Title: EIF4A3-induced circ_0084615 contributes to the progression of colorectal cancer via miR-599/ONECUT2 pathway
    Article Snippet: assay was performed as previously reported [ ]. .. The antibodies against ONECUT2 (bs-19643R), ZEB2 (bs-20484R), E-cadherin (bs-1519R), Vimentin (bs-0756R) and VEGFA (bs-20393R) were bought from Bioss.



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    Image Search Results


    OC2 knockdown inhibited proliferation and promoted apoptosis in HCC cells. A - B The expression of OC2 in HCC clinical samples was analyzed by qRT‒PCR and Western blotting. “T” represents tumor tissue, and “N” represents normal tissue. C The expression of OC2 in HCC clinical tissues was analyzed by IHC. Scale bar: 200 μm. D - E The expression of OC2 in normal cells (HEK293T and HUVEC) and HCC cells (SK-Hep1, PLC/PRF/5, Huh6 and HepG2) was analyzed by qRT‒PCR and Western blotting. F - G Results of qRT‒PCR and Western blot analysis of the effects of OC2 interference by shRNA (OC2 knockdown) in HCC cells. H - I Results of the CCK-8 and plate colony formation assays with OC2 knockdown in HCC cells. J The phosphorylation levels of AKT and MAPK and the expression of FGF2 in HCC cells were analyzed by Western blotting. K The apoptosis of HCC cells with OC2 knockdown was analyzed by flow cytometry. L - M The expression of apoptosis-related factors (PARP, Bcl2 and Bax) in HCC cells was analyzed by qRT‒PCR and Western blotting. The data are expressed as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: OC2 knockdown inhibited proliferation and promoted apoptosis in HCC cells. A - B The expression of OC2 in HCC clinical samples was analyzed by qRT‒PCR and Western blotting. “T” represents tumor tissue, and “N” represents normal tissue. C The expression of OC2 in HCC clinical tissues was analyzed by IHC. Scale bar: 200 μm. D - E The expression of OC2 in normal cells (HEK293T and HUVEC) and HCC cells (SK-Hep1, PLC/PRF/5, Huh6 and HepG2) was analyzed by qRT‒PCR and Western blotting. F - G Results of qRT‒PCR and Western blot analysis of the effects of OC2 interference by shRNA (OC2 knockdown) in HCC cells. H - I Results of the CCK-8 and plate colony formation assays with OC2 knockdown in HCC cells. J The phosphorylation levels of AKT and MAPK and the expression of FGF2 in HCC cells were analyzed by Western blotting. K The apoptosis of HCC cells with OC2 knockdown was analyzed by flow cytometry. L - M The expression of apoptosis-related factors (PARP, Bcl2 and Bax) in HCC cells was analyzed by qRT‒PCR and Western blotting. The data are expressed as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Knockdown, Expressing, Western Blot, shRNA, CCK-8 Assay, Phospho-proteomics, Flow Cytometry

    OC2 knockout inhibited proliferation and migration and promoted apoptosis. A Recognition sites of sgRNA1 and sgRNA2 in exon 1 of the OC2 gene. B - C The relative expression of OC2 in B8 and B10 cells was analyzed by Western blotting and qRT‒PCR. The “blank” group consisted of SK-Hep1 cells that were not transfected with lentivirus; the “Con” (Control) group consisted of SK-Hep1 cells that were transfected with lentivirus without a knockout site; the “B8” and “B10” groups consisted of SK-Hep1 cells that were transfected with lentivirus containing the sgRNA1 and sgRNA2 knockout sites. D - E The proliferation of B8 and B10 cells was analyzed by CCK-8 and plate colony formation assays. F The expression of ATK, MAPK, and FGF2 in B8 and B10 cells was analyzed by qRT‒PCR. G The phosphorylation levels of ATK and MAPK and the expression of FGF2 in B8 and B10 cells was analyzed by Western blotting. H Tube formation assay of HUVECs treated with the supernatant of B8 and B10 cells. Scale bar: 100 μm. I - J The expression of angiogenesis-related factors (CD31, PDGF-B, VEGFA, angiogenin and TGF-β1) in B8 and B10 cells was analyzed by qRT‒PCR and Western blotting. K Apoptosis results from the flow cytometry assay in B8 and B10 cells. L - M The expression of apoptosis-related factors in B8 and B10 cells was analyzed by qRT‒PCR and Western blotting. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: OC2 knockout inhibited proliferation and migration and promoted apoptosis. A Recognition sites of sgRNA1 and sgRNA2 in exon 1 of the OC2 gene. B - C The relative expression of OC2 in B8 and B10 cells was analyzed by Western blotting and qRT‒PCR. The “blank” group consisted of SK-Hep1 cells that were not transfected with lentivirus; the “Con” (Control) group consisted of SK-Hep1 cells that were transfected with lentivirus without a knockout site; the “B8” and “B10” groups consisted of SK-Hep1 cells that were transfected with lentivirus containing the sgRNA1 and sgRNA2 knockout sites. D - E The proliferation of B8 and B10 cells was analyzed by CCK-8 and plate colony formation assays. F The expression of ATK, MAPK, and FGF2 in B8 and B10 cells was analyzed by qRT‒PCR. G The phosphorylation levels of ATK and MAPK and the expression of FGF2 in B8 and B10 cells was analyzed by Western blotting. H Tube formation assay of HUVECs treated with the supernatant of B8 and B10 cells. Scale bar: 100 μm. I - J The expression of angiogenesis-related factors (CD31, PDGF-B, VEGFA, angiogenin and TGF-β1) in B8 and B10 cells was analyzed by qRT‒PCR and Western blotting. K Apoptosis results from the flow cytometry assay in B8 and B10 cells. L - M The expression of apoptosis-related factors in B8 and B10 cells was analyzed by qRT‒PCR and Western blotting. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Knock-Out, Migration, Expressing, Western Blot, Transfection, Control, CCK-8 Assay, Phospho-proteomics, Tube Formation Assay, Flow Cytometry

    Identification of OC2-binding genes via ChIP‒Seq, qRT‒PCR and ChIP‒qPCR. A - B The relative expression of candidate genes analyzed by qRT‒PCR after OC2 was overexpressed in HepG2 and SK-Hep1 cells. The “OENC” group consisted of SK-Hep1 or HepG2 cells transfected with overexpression empty plasmid; The “OEOC2” group consisted of SK-Hep1 or HepG2 cells transfected with OC2-overexpressing plasmid; C The relative expression of candidate genes analyzed by qRT‒PCR in B8 cells. The “NC” group consisted of SK-Hep1 cells that were transfected with lentivirus without a knockout site; the “B8” group consisted of SK-Hep1 cells with OC2 knockout. D The promoter activities of DSP and SKP2 were analyzed via dual-luciferase reporter assays. The “pGL3-Basic” group consisted of SK-Hep1 cells transfected with an empty plasmid without the promoter sequence inserted; The “pGL3-DSP” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the DSP promoter sequence; The “pGL3-SKP2” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the SKP2 promoter sequence. E Motif of the OC2 transcription factor binding to DNA. F Mutations in the OC2 binding site in the SKP2 promoter sequence. The bases marked in red are the base sequences after mutation. G The mutant promoter activity of SKP2 was analyzed via dual-luciferase reporter assays. The “pGL3-SKP2-WT” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the normal SKP2 promoter sequence; The “pGL3-SKP2-mut” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the mutated SKP2 promoter sequence. H - I The expression of SKP2 in HCC clinical samples was analyzed by Western blotting and qRT‒PCR. J Correlation analysis of the relative expression levels of OC2 and SKP2 in HCC clinical samples. K The relative expression of SKP2 after OC2 knockdown in HepG2 and SK-Hep1 cells was analyzed by Western blotting. L Relative fold enrichment of SKP2 promoter fragments analyzed by ChIP‒qPCR in HepG2 and SK-Hep1 cells. The “IgG” group was immunoprecipitated using anti-IgG antibody; the “OENC” and “OEOC2” groups were immunoprecipitated using anti-OC2 antibody. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: Identification of OC2-binding genes via ChIP‒Seq, qRT‒PCR and ChIP‒qPCR. A - B The relative expression of candidate genes analyzed by qRT‒PCR after OC2 was overexpressed in HepG2 and SK-Hep1 cells. The “OENC” group consisted of SK-Hep1 or HepG2 cells transfected with overexpression empty plasmid; The “OEOC2” group consisted of SK-Hep1 or HepG2 cells transfected with OC2-overexpressing plasmid; C The relative expression of candidate genes analyzed by qRT‒PCR in B8 cells. The “NC” group consisted of SK-Hep1 cells that were transfected with lentivirus without a knockout site; the “B8” group consisted of SK-Hep1 cells with OC2 knockout. D The promoter activities of DSP and SKP2 were analyzed via dual-luciferase reporter assays. The “pGL3-Basic” group consisted of SK-Hep1 cells transfected with an empty plasmid without the promoter sequence inserted; The “pGL3-DSP” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the DSP promoter sequence; The “pGL3-SKP2” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the SKP2 promoter sequence. E Motif of the OC2 transcription factor binding to DNA. F Mutations in the OC2 binding site in the SKP2 promoter sequence. The bases marked in red are the base sequences after mutation. G The mutant promoter activity of SKP2 was analyzed via dual-luciferase reporter assays. The “pGL3-SKP2-WT” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the normal SKP2 promoter sequence; The “pGL3-SKP2-mut” group consisted of SK-Hep1 cells transfected with a plasmid inserted with the mutated SKP2 promoter sequence. H - I The expression of SKP2 in HCC clinical samples was analyzed by Western blotting and qRT‒PCR. J Correlation analysis of the relative expression levels of OC2 and SKP2 in HCC clinical samples. K The relative expression of SKP2 after OC2 knockdown in HepG2 and SK-Hep1 cells was analyzed by Western blotting. L Relative fold enrichment of SKP2 promoter fragments analyzed by ChIP‒qPCR in HepG2 and SK-Hep1 cells. The “IgG” group was immunoprecipitated using anti-IgG antibody; the “OENC” and “OEOC2” groups were immunoprecipitated using anti-OC2 antibody. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Binding Assay, Expressing, Transfection, Over Expression, Plasmid Preparation, Knock-Out, Luciferase, Sequencing, Mutagenesis, Activity Assay, Western Blot, Knockdown, Immunoprecipitation

    SKP2 knockdown inhibited proliferation and promoted apoptosis in HCC cells. A - B SKP2 knockdown with shRNA in HepG2 and SK-Hep1 cells was analyzed by qRT‒PCR and Western blotting. C SKP2 knockdown inhibited the proliferation of HepG2 and SK-Hep1 cells, as determined by CCK-8 assays. D SKP2 knockdown promoted the apoptosis of HepG2 and SK-Hep1 cells, as determined by flow cytometry. E - F SKP2 knockdown increased the expression of apoptosis-related factors, as determined by qRT‒PCR and Western blotting, in HepG2 and SK-Hep1 cells. G - H SKP2 knockdown promoted the expression of p21 and p27, as determined by qRT‒PCR and Western blotting, in HepG2 and SK-Hep1 cells. I OC2 knockdown increased the expression of p21 and p27, as determined by Western blotting, in HepG2 and SK-Hep1 cells. The data are expressed as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: SKP2 knockdown inhibited proliferation and promoted apoptosis in HCC cells. A - B SKP2 knockdown with shRNA in HepG2 and SK-Hep1 cells was analyzed by qRT‒PCR and Western blotting. C SKP2 knockdown inhibited the proliferation of HepG2 and SK-Hep1 cells, as determined by CCK-8 assays. D SKP2 knockdown promoted the apoptosis of HepG2 and SK-Hep1 cells, as determined by flow cytometry. E - F SKP2 knockdown increased the expression of apoptosis-related factors, as determined by qRT‒PCR and Western blotting, in HepG2 and SK-Hep1 cells. G - H SKP2 knockdown promoted the expression of p21 and p27, as determined by qRT‒PCR and Western blotting, in HepG2 and SK-Hep1 cells. I OC2 knockdown increased the expression of p21 and p27, as determined by Western blotting, in HepG2 and SK-Hep1 cells. The data are expressed as mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Knockdown, shRNA, Western Blot, CCK-8 Assay, Flow Cytometry, Expressing

    Role of proliferation and apoptosis mediated by the overexpression of OC2 and SKP2 in B8 cells. A The proliferation of B8 cells overexpressing OC2 was analyzed via a CCK-8 assay. B Flow cytometry assay of apoptosis levels in B8 cells overexpressing OC2. C The expression of apoptosis-related factors (SKP2, PARP, Bax, Bcl2, p21 and p27) in B8 cells overexpressing OC2. D Proliferation of B8 cells overexpressing SKP2. E Flow cytometry assay of apoptosis levels in B8 cells overexpressing SKP2. F - G The expression of apoptosis-related factors in B8 cells overexpressing SKP2 was analyzed by Western blotting and qRT‒PCR. H The phosphorylation and acetylation levels of p53 were analyzed by Western blotting in B8 cells overexpressing SKP2. I Dual-luciferase reporter assays of p53 response element-related fluorescence activity in SK-Hep1 cells with OC2 and SKP2 knockdown. The “p53-RE” group consisted of SK-Hep1 cells transfected with pGPL3-Basic plasmid with p53 response element sequence inserted. J Phosphorylation and acetylation levels of p53 in B8 cells overexpressing OC2 and SKP2. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: Role of proliferation and apoptosis mediated by the overexpression of OC2 and SKP2 in B8 cells. A The proliferation of B8 cells overexpressing OC2 was analyzed via a CCK-8 assay. B Flow cytometry assay of apoptosis levels in B8 cells overexpressing OC2. C The expression of apoptosis-related factors (SKP2, PARP, Bax, Bcl2, p21 and p27) in B8 cells overexpressing OC2. D Proliferation of B8 cells overexpressing SKP2. E Flow cytometry assay of apoptosis levels in B8 cells overexpressing SKP2. F - G The expression of apoptosis-related factors in B8 cells overexpressing SKP2 was analyzed by Western blotting and qRT‒PCR. H The phosphorylation and acetylation levels of p53 were analyzed by Western blotting in B8 cells overexpressing SKP2. I Dual-luciferase reporter assays of p53 response element-related fluorescence activity in SK-Hep1 cells with OC2 and SKP2 knockdown. The “p53-RE” group consisted of SK-Hep1 cells transfected with pGPL3-Basic plasmid with p53 response element sequence inserted. J Phosphorylation and acetylation levels of p53 in B8 cells overexpressing OC2 and SKP2. The data are expressed as mean ± SD; “ns” indicates no significant difference; * P < 0.05, ** P < 0.01, *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Over Expression, CCK-8 Assay, Flow Cytometry, Expressing, Western Blot, Phospho-proteomics, Luciferase, Fluorescence, Activity Assay, Knockdown, Transfection, Plasmid Preparation, Sequencing

    Effect of OC2 knockout on tumor growth in vivo. A Schematic diagram of the xenograft mouse model. The volume of the tumor was measured every three days after the tumor was subcutaneously formed in the mouse. B Tumor tissues were removed from the mice in the B8 and B10 cell groups and the control group. C - D Tumor growth curves and tumor weights. E The phosphorylation levels of AKT and MAPK and the expression of FGF2 in tumor tissues were analyzed by Western blotting. F The expression of angiogenesis-related factors in tumor tissues was analyzed by Western blotting. G The expression of apoptosis-related factors in tumor tissues was analyzed by Western blotting. H Results of immunohistochemistry and TUNEL assays for tumor growth and apoptosis. Scale bar: 100 μm; the data are expressed as mean ± SD; *** P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: Effect of OC2 knockout on tumor growth in vivo. A Schematic diagram of the xenograft mouse model. The volume of the tumor was measured every three days after the tumor was subcutaneously formed in the mouse. B Tumor tissues were removed from the mice in the B8 and B10 cell groups and the control group. C - D Tumor growth curves and tumor weights. E The phosphorylation levels of AKT and MAPK and the expression of FGF2 in tumor tissues were analyzed by Western blotting. F The expression of angiogenesis-related factors in tumor tissues was analyzed by Western blotting. G The expression of apoptosis-related factors in tumor tissues was analyzed by Western blotting. H Results of immunohistochemistry and TUNEL assays for tumor growth and apoptosis. Scale bar: 100 μm; the data are expressed as mean ± SD; *** P < 0.001

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Knock-Out, In Vivo, Control, Phospho-proteomics, Expressing, Western Blot, Immunohistochemistry, TUNEL Assay

    The mechanism by which OC2 regulates proliferation and apoptosis in HCC cells. OC2 promoted the transcriptional activation of SKP2, which inhibited the binding of p53 to p300 and downregulated the acetylation level of p53, thereby inhibiting the apoptosis of HCC cells. The solid line indicates direct action; the dotted line indicates indirect action; the “AC” indicates acetylation; the “P” indicates phosphorylation

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Knockout of onecut2 inhibits proliferation and promotes apoptosis of tumor cells through SKP2-mediated p53 acetylation in hepatocellular carcinoma

    doi: 10.1007/s00018-024-05518-3

    Figure Lengend Snippet: The mechanism by which OC2 regulates proliferation and apoptosis in HCC cells. OC2 promoted the transcriptional activation of SKP2, which inhibited the binding of p53 to p300 and downregulated the acetylation level of p53, thereby inhibiting the apoptosis of HCC cells. The solid line indicates direct action; the dotted line indicates indirect action; the “AC” indicates acetylation; the “P” indicates phosphorylation

    Article Snippet: The sections were incubated with primary antibodies against OC2 (Proteintech, 21916-1-AP, 1:250), SKP2 (Cell Signaling Technology, 2652, 1:200), KI67 (Cell Signaling Technology, 12202, 1:400) and CD31 (Cell Signaling Technology, 77699, 1:200) at 4 °C overnight.

    Techniques: Activation Assay, Binding Assay, Phospho-proteomics

    Figure 3. ONECUT2 signalling in M cell precursor cluster. (A) On the left, UMAP embedding overlay showing three partitions, group of interest 1 (GOI1), 2 (GOI2) and 3 (GOI3). On the right, top four transcription factors expressed within GOI1, with the highest positive correlation between transcript factor expression and motif activity. The logos for the motif of HNF4G (GM.5.0.Nuclear receptor.0068), KLF5 (GM.5.0.C2H2 ZF.0006), ONECUT2 (GM.5.0.CUT Homeodomain.0005) and TCF7L2 (GM.5.0.Mixed.0092) are displayed. (B) ONECUT2 ChIPmentation signal and DNA accessibility (from ATAC sequencing) at shared or RANKL-specific ONECUT2 binding sites. From ChIPmentation, heatmap shows one representative replicate for each condition as well as input signal for RANKL and control samples. (C) Gene-regulatory network of Onecut2 drivers predicted by ANANSE. Interaction scores (arbitrary cut-off ≥0.83) are depicted. (D) Trajectory plot overlaid with cluster identity of individual cells from RANKL-treated clusters in GOI1. Three major branches are shown along the plot. On the right, same trajectory plot with cells ordered along a pseudotime. Below, log10 expression values of Onecut2 and top genes from each branching point are shown. (E) Co-regulated modules of differentially expressed genes by cells from RANKL-treated clusters in GOI1. The transcription factors predicted by ANANSE as Onecut2 drivers and ONECUT2 targets, that are differentially expressed (Padj < 0.05) by cells from RANKL-treated clusters within GOI1 and defined as pseudotime-dependent genes are highlighted.

    Journal: Nucleic acids research

    Article Title: ONECUT2 regulates RANKL-dependent enterocyte and microfold cell differentiation in the small intestine; a multi-omics study.

    doi: 10.1093/nar/gkac1236

    Figure Lengend Snippet: Figure 3. ONECUT2 signalling in M cell precursor cluster. (A) On the left, UMAP embedding overlay showing three partitions, group of interest 1 (GOI1), 2 (GOI2) and 3 (GOI3). On the right, top four transcription factors expressed within GOI1, with the highest positive correlation between transcript factor expression and motif activity. The logos for the motif of HNF4G (GM.5.0.Nuclear receptor.0068), KLF5 (GM.5.0.C2H2 ZF.0006), ONECUT2 (GM.5.0.CUT Homeodomain.0005) and TCF7L2 (GM.5.0.Mixed.0092) are displayed. (B) ONECUT2 ChIPmentation signal and DNA accessibility (from ATAC sequencing) at shared or RANKL-specific ONECUT2 binding sites. From ChIPmentation, heatmap shows one representative replicate for each condition as well as input signal for RANKL and control samples. (C) Gene-regulatory network of Onecut2 drivers predicted by ANANSE. Interaction scores (arbitrary cut-off ≥0.83) are depicted. (D) Trajectory plot overlaid with cluster identity of individual cells from RANKL-treated clusters in GOI1. Three major branches are shown along the plot. On the right, same trajectory plot with cells ordered along a pseudotime. Below, log10 expression values of Onecut2 and top genes from each branching point are shown. (E) Co-regulated modules of differentially expressed genes by cells from RANKL-treated clusters in GOI1. The transcription factors predicted by ANANSE as Onecut2 drivers and ONECUT2 targets, that are differentially expressed (Padj < 0.05) by cells from RANKL-treated clusters within GOI1 and defined as pseudotime-dependent genes are highlighted.

    Article Snippet: Then, chromatin of each replicate was incubated with 1 g of antibody against H3K27ac (Diagenode, C15410196, RRID: AB 2637079) or 1 g of antibody against ONECUT2 (Proteintech, 21916-1-AP, AB 2848180) in dilution buffer (1% Triton X-100, 1.2 mM EDTA, 16.7 mM Tris pH 8, 167 mM NaCl, 1× Protease Inhibitor Cocktail (Roche)), rotating overnight at 4◦C.

    Techniques: Expressing, Activity Assay, Sequencing, Binding Assay, Control

    miR-429 targets transcript factor Onecut2 and is inversely correlated with the mRNA or protein levels of Onecut2 in CRC tissues. a Luciferase assay on SW620 cells, which were cotransfected with miR-429 and a luciferase reporter containing the full length of Onecut2 3′-UTR (Luc-wt) or a mutant (Luc-mut) in which the four nucleotides of the miR-429-binding site were mutated. Luciferase activities were measured 48-h post transfection. miR-429 markedly suppressed luciferase activity in Luc-wt reporter constructs. The data are mean ± SD for separate transfections ( n = 6). b Onecut2 mRNA level was analyzed upon miR-429 or scramble transfection in HT-29, SW620, and SW480 cells by real-time PCR. All data are shown as mean ± SD. ** P < 0.01. c miR-429 transfection affects Onecut2 protein levels by Western blot analysis. HT-29, SW620, and SW480 cells were transfected with miR-429 or scramble control. d Representative expression levels of miR429 and Onecut2 mRNA by real-time PCR in clinical specimens ( n = 50), and the correlation between miR-429 and Onecut2 was analyzed by Spearman’s correlation test. e ISH detects the position and expression of miR-429, and IHC detects the position and expression of Onecut2 in CRC (103 cases) relative to paracancerous normal tissues (103 cases). Scale bars 100 μm

    Journal: Molecular and Cellular Biochemistry

    Article Title: miR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma

    doi: 10.1007/s11010-013-1950-x

    Figure Lengend Snippet: miR-429 targets transcript factor Onecut2 and is inversely correlated with the mRNA or protein levels of Onecut2 in CRC tissues. a Luciferase assay on SW620 cells, which were cotransfected with miR-429 and a luciferase reporter containing the full length of Onecut2 3′-UTR (Luc-wt) or a mutant (Luc-mut) in which the four nucleotides of the miR-429-binding site were mutated. Luciferase activities were measured 48-h post transfection. miR-429 markedly suppressed luciferase activity in Luc-wt reporter constructs. The data are mean ± SD for separate transfections ( n = 6). b Onecut2 mRNA level was analyzed upon miR-429 or scramble transfection in HT-29, SW620, and SW480 cells by real-time PCR. All data are shown as mean ± SD. ** P < 0.01. c miR-429 transfection affects Onecut2 protein levels by Western blot analysis. HT-29, SW620, and SW480 cells were transfected with miR-429 or scramble control. d Representative expression levels of miR429 and Onecut2 mRNA by real-time PCR in clinical specimens ( n = 50), and the correlation between miR-429 and Onecut2 was analyzed by Spearman’s correlation test. e ISH detects the position and expression of miR-429, and IHC detects the position and expression of Onecut2 in CRC (103 cases) relative to paracancerous normal tissues (103 cases). Scale bars 100 μm

    Article Snippet: Rabbit polyclonal primary antibody against Onecut2 and mouse monoclonal antibody GAPDH was purchased from Cell Signaling Technology (Beverly, MA, USA) and Santa Cruz Biotechnology Inc., (Santa Cruz, CA).

    Techniques: Luciferase, Mutagenesis, Binding Assay, Transfection, Activity Assay, Construct, Real-time Polymerase Chain Reaction, Western Blot, Control, Expressing

    Effect of miR-429 on cells mobility and invasion by target Onecut2 in CRC cells. a Wound-healing assay analyzes the effect of miR-429 or si-Onecut2 on SW620 cells migration. * P < 0.05. b Wound-healing assay analyzes the rescued effect of Onecut2 overexpression on inhibitory healing induced by miR-429. * P < 0.05. c Matrigel invasion assay analyzes the rescued effect of Onecut2 overexpression on invasion inhibition induced by miR-429. ** P < 0.01

    Journal: Molecular and Cellular Biochemistry

    Article Title: miR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma

    doi: 10.1007/s11010-013-1950-x

    Figure Lengend Snippet: Effect of miR-429 on cells mobility and invasion by target Onecut2 in CRC cells. a Wound-healing assay analyzes the effect of miR-429 or si-Onecut2 on SW620 cells migration. * P < 0.05. b Wound-healing assay analyzes the rescued effect of Onecut2 overexpression on inhibitory healing induced by miR-429. * P < 0.05. c Matrigel invasion assay analyzes the rescued effect of Onecut2 overexpression on invasion inhibition induced by miR-429. ** P < 0.01

    Article Snippet: Rabbit polyclonal primary antibody against Onecut2 and mouse monoclonal antibody GAPDH was purchased from Cell Signaling Technology (Beverly, MA, USA) and Santa Cruz Biotechnology Inc., (Santa Cruz, CA).

    Techniques: Wound Healing Assay, Migration, Over Expression, Invasion Assay, Inhibition

    miR-429 regulates the expression of EMT-related marker genes by targeting Onecut2 in CRC cells. a miR-429 rescued the expression alteration of EMT-related marker genes induced by TGF-β1 in SW620 cells. * P < 0.05. b si-Onecut2 rescued the expression alteration of EMT-related marker genes induced by TGF-β1 in SW620 cells. * P < 0.05

    Journal: Molecular and Cellular Biochemistry

    Article Title: miR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma

    doi: 10.1007/s11010-013-1950-x

    Figure Lengend Snippet: miR-429 regulates the expression of EMT-related marker genes by targeting Onecut2 in CRC cells. a miR-429 rescued the expression alteration of EMT-related marker genes induced by TGF-β1 in SW620 cells. * P < 0.05. b si-Onecut2 rescued the expression alteration of EMT-related marker genes induced by TGF-β1 in SW620 cells. * P < 0.05

    Article Snippet: Rabbit polyclonal primary antibody against Onecut2 and mouse monoclonal antibody GAPDH was purchased from Cell Signaling Technology (Beverly, MA, USA) and Santa Cruz Biotechnology Inc., (Santa Cruz, CA).

    Techniques: Expressing, Marker

    The primers of EMT-related marker genes

    Journal: Molecular and Cellular Biochemistry

    Article Title: miR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma

    doi: 10.1007/s11010-013-1950-x

    Figure Lengend Snippet: The primers of EMT-related marker genes

    Article Snippet: Rabbit polyclonal primary antibody against Onecut2 and mouse monoclonal antibody GAPDH was purchased from Cell Signaling Technology (Beverly, MA, USA) and Santa Cruz Biotechnology Inc., (Santa Cruz, CA).

    Techniques: Marker