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cdk4 6 inhibitors  (MedChemExpress)


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    Structured Review

    MedChemExpress cdk4 6 inhibitors
    NEK6 knockout enhanced the efficiency <t>of</t> <t>CDK4/6</t> inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
    Cdk4 6 Inhibitors, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 78 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cdk4 6 inhibitors/product/MedChemExpress
    Average 95 stars, based on 78 article reviews
    cdk4 6 inhibitors - by Bioz Stars, 2026-02
    95/100 stars

    Images

    1) Product Images from "Genome-wide CRISPR screen identified NEK6 as a determinant of sensitivity to CDK4/6 inhibitor in endometrial cancer"

    Article Title: Genome-wide CRISPR screen identified NEK6 as a determinant of sensitivity to CDK4/6 inhibitor in endometrial cancer

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2025.1725886

    NEK6 knockout enhanced the efficiency of CDK4/6 inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
    Figure Legend Snippet: NEK6 knockout enhanced the efficiency of CDK4/6 inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.

    Techniques Used: Knock-Out, Single Cell Gel Electrophoresis, Concentration Assay, Immunofluorescence, Staining, Western Blot, Knockdown, Flow Cytometry

    The proposed model elaborating the mechanisms underlying NEK6 depletion enhanced CDK4/6 inhibitors sensitivity in EC.
    Figure Legend Snippet: The proposed model elaborating the mechanisms underlying NEK6 depletion enhanced CDK4/6 inhibitors sensitivity in EC.

    Techniques Used:



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    NEK6 knockout enhanced the efficiency <t>of</t> <t>CDK4/6</t> inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
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    Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, <t>CDK4,</t> and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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    Image Search Results


    NEK6 knockout enhanced the efficiency of CDK4/6 inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.

    Journal: Frontiers in Pharmacology

    Article Title: Genome-wide CRISPR screen identified NEK6 as a determinant of sensitivity to CDK4/6 inhibitor in endometrial cancer

    doi: 10.3389/fphar.2025.1725886

    Figure Lengend Snippet: NEK6 knockout enhanced the efficiency of CDK4/6 inhibitor-induced DNA damage repair and apoptosis. (A) DNA damage detected by comet assay in HEC-1A cells (siNC or si-NEK6) treated with indicated concentration of palbociclib. Scale bar, 50 μm. Quantification of DNA in the tail from three independent experiments is shown as mean ± s.d. (B) Immunofluorescence staining of γ-H2AX in sh-NC and sh-NEK6 HEC-1A and Ishikawa cells treated with or without palbociclib. Scale bar = 10 μm. (C) Western blot analysis of phosphorylated H2AX and RAD51 in HEC-1A and ishikawa endometrial cancer cells treated as indicated. (D) Knockdown of NEK6 induced apoptosis significantly upon palbociclib treatment in HEC-1A evaluated by flow cytometry analysis. Data were presented as the mean ± s.d. of values obtained in 3 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.

    Article Snippet: The CDK4/6 inhibitors (abemaciclib, palbociclib, ribociclib) and the specific NEK6 inhibitor ZINC05007751 was purchased from MedChem Express (Shanghai, China).

    Techniques: Knock-Out, Single Cell Gel Electrophoresis, Concentration Assay, Immunofluorescence, Staining, Western Blot, Knockdown, Flow Cytometry

    The proposed model elaborating the mechanisms underlying NEK6 depletion enhanced CDK4/6 inhibitors sensitivity in EC.

    Journal: Frontiers in Pharmacology

    Article Title: Genome-wide CRISPR screen identified NEK6 as a determinant of sensitivity to CDK4/6 inhibitor in endometrial cancer

    doi: 10.3389/fphar.2025.1725886

    Figure Lengend Snippet: The proposed model elaborating the mechanisms underlying NEK6 depletion enhanced CDK4/6 inhibitors sensitivity in EC.

    Article Snippet: The CDK4/6 inhibitors (abemaciclib, palbociclib, ribociclib) and the specific NEK6 inhibitor ZINC05007751 was purchased from MedChem Express (Shanghai, China).

    Techniques:

    Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, CDK4, and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: A promising magnesium-related alloy with metabolic reprogramming and antitumor effects in hepatocellular and pancreatic cancer

    doi: 10.1016/j.bioactmat.2025.12.039

    Figure Lengend Snippet: Metabolomic Analysis Reveals Mg and Al-Mg Induce Metabolic Reprogramming in Hepatocellular and Pancreatic Cancer Cells. (A) Metabolomic profiling of PANC-1, PANC-1-Mg, PANC-1-Al-Mg, Huh7, Huh7-Mg, and Huh7-Al-Mg groups using LC-MS identified 1824 metabolites. (B) PCA illustrating clustering among different cell groups. (C) Heatmap showing differential abundances of characteristic metabolites across cell groups. (D) K-means clustering analysis highlighting metabolic differences among the cell groups. (E) Venn diagram displaying common differential metabolites among treatment groups. (F) Volcano plots of differential metabolites following Mg or Al-Mg treatment. (G) KEGG pathway enrichment analysis of differential metabolites. (H) Enrichment distribution of differential metabolites in Huh7 or PANC-1 cells treated with Mg or Al-Mg. (I) Quantitative analysis of intracellular metabolites including L-glutamine, adenine, uridine, cytidine, and guanine by ELISA with Mg or Al-Mg exposure. (J) Western blot analysis of p21, CDK4, and PCNA expression in PANC-1 cells after Mg or Al-Mg exposure. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After blocking with 5 % nonfat milk for 1 h at room temperature, membranes were incubated overnight at 4 °C with primary antibodies, including AMPK (1:1000, CST, 2532), p-AMPK (1:1000, CST, 2535), CPT1B (1:1000, Proteintech, 22170-1-AP), CDK4 (1:1000, Proteintech, 11026-1-AP), PCNA (1:1000, Proteintech, 10205-2-AP), p21 (1:1000, Proteintech, 10355-1-AP), GAPDH (1:1000, Proteintech, 60004-1-Ig) followed by HRP-conjugated secondary antibody (1:5000, Proteintech, RGAR001) for 1 h at room temperature.

    Techniques: Liquid Chromatography with Mass Spectroscopy, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing