Journal: Frontiers in Pharmacology

Article Title: Integrated multi-omics analysis suggests the involvement of PI3K-Akt/p21 signaling in the anti-colorectal cancer effects of Diaphragma Juglandis Fructus extract

doi: 10.3389/fphar.2026.1833123

Figure Lengend Snippet: EEDJF induces G1/S cell cycle arrest in HCT116 cells. (A) Western blot analysis of cell cycle–related proteins (p21, Cyclin D1, and CDK4) following EEDJF treatment. (B) Densitometric quantification of protein expression shown in (A) . Band intensities were quantified using ImageJ software and normalized to β-actin. (C) Flow cytometric analysis of cell cycle distribution after EEDJF treatment. (D,E) Quantitative distribution of cells in G1, S, and G2/M phases. Data are presented as mean ± SD from three independent biological experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Antibodies were purchased as follows: p-PI3K from Bioss (Beijing, China); PI3K and p21 from Proteintech (Wuhan, China); p-Akt, Cyclin D1, and CDK4 from Wanleibio (Shenyang, China); and total AKT from Cell Signaling Technology (MA, USA).

Techniques: Western Blot, Expressing, Software

Journal: Cancer Medicine

Article Title: Artesunate Induces G0 / G1 Phase Arrest in Tumor Cells and Associates With Cyclin‐Dependent Kinase 4 ( CDK4 )

doi: 10.1002/cam4.71907

Figure Lengend Snippet: CDK4 is directly targeted by artesunate. (A) Schematic of artesunate target screening using a HuProt proteome microarray. (B) Venn diagram analysis. (C) CDK4 had the highest IMean_Ratio value. (D) Molecular docking analysis. Detailed protein names and Ratio values are provided in Tables and , respectively.

Article Snippet: Recombinant human CDK4 protein (Cat # HY‐P702860) was purchased from MedChemExpress (Shanghai, China).

Techniques: Microarray

Journal: Cancer Medicine

Article Title: Artesunate Induces G0 / G1 Phase Arrest in Tumor Cells and Associates With Cyclin‐Dependent Kinase 4 ( CDK4 )

doi: 10.1002/cam4.71907

Figure Lengend Snippet: Artesunate induces G0/G1 phase arrest and suppresses the CDK4–Cyclin D1–Rb–E2F1 pathway in NSCLC cells. (A) The dose–response curve of artesunate‐CDK4. (B) SPR analysis on the interactions between artesunate and CDK4. (C) Flow cytometry analysis showing G0/G1 phase accumulation in A549 and H1299 cells after 48 h of treatment with different concentrations of artesunate. (D) Western blot analysis of key CDK4/6–Cyclin D1–Rb–E2F1 pathway proteins in treated A549 and H1299 cells. The data are presented as the mean ± SD. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001; Student's t test. Uncropped images are provided in Figures and .

Article Snippet: Recombinant human CDK4 protein (Cat # HY‐P702860) was purchased from MedChemExpress (Shanghai, China).

Techniques: Flow Cytometry, Western Blot

Journal: Cancer Medicine

Article Title: Artesunate Induces G0 / G1 Phase Arrest in Tumor Cells and Associates With Cyclin‐Dependent Kinase 4 ( CDK4 )

doi: 10.1002/cam4.71907

Figure Lengend Snippet: Schematic diagram showing the mechanism by which artesunate regulates the CDK4–Cyclin D1–Rb–E2F1 pathway.

Article Snippet: Recombinant human CDK4 protein (Cat # HY‐P702860) was purchased from MedChemExpress (Shanghai, China).

Techniques:

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

Journal: bioRxiv

Article Title: CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

doi: 10.64898/2026.04.19.719504

Figure Lengend Snippet: ( A ) Representative flow cytometry plots showing surface expression of indicated NK cell-activating and inhibiting signals in a PDO158 treated with 1 μM abemaciclib or vehicle control for 5 days. ( B ) Quantification of surface marker expression across 11 PDOs treated as in (A). n=3. ***p < 0.001, ****p < 0.0001 (two-way ANOVA). ( C ) Pie chart showing the proportion of PDOs that upregulated stress ligands and ICAM-1 after CDK4/6i treatment based on data in (B).

Article Snippet: Small molecule inhibitors, including CDK4/6i abemaciclib and ribociclib, PI3K/mTORi gedatolisib, and NFkB inhibitor BMS-345541 were purchased from AdooQ, MedChemExpress, and Selleckchem.

Techniques: Flow Cytometry, Expressing, Control, Marker

Journal: bioRxiv

Article Title: CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

doi: 10.64898/2026.04.19.719504

Figure Lengend Snippet: ( A, B ) Schematic of in vivo experiments administering CDK4/6i and NK cells sequentially (A) or concurrently (B). For sequential treatment (experiments 1 and 2, C-F), mice were pretreated with abemaciclib for 7-11 days, followed by a single NK cell infusion (10×10⁶ cells/injection). For concurrent treatment (experiment 3, G-H), mice were pretreated with abemaciclib for one week, and abemaciclib and NK cells (10×10⁶ cells/injection, weekly) were administered simultaneously. ( C ) Experiment 1, sequential treatment. Tumor growth curves in PDX-bearing mice treated with abemaciclib (75 mg/kg, daily) and NK92 cells. The treatment schedule is as shown in (A). n = 5 mice/group. Statistical significance calculated using 2-way ANOVA with Tukey’s post-test. ( D ) Corresponding survival curves for the experiment in (C). The Log-rank (Mantel-Cox) test was used to compare the combo and vehicle groups. ( E-F ) Tumor growth and survival in Experiment 2 with sequential treatment. The treatment scheme is shown in (A). Doses and analyses as in (C-D). n = 5 mice/group. ( G-H ) Tumor growth and survival in Experiment 3 with concurrent treatment. The treatment scheme is shown in (B). Doses and analyses as in (C-D). n = 5 mice/group.

Article Snippet: Small molecule inhibitors, including CDK4/6i abemaciclib and ribociclib, PI3K/mTORi gedatolisib, and NFkB inhibitor BMS-345541 were purchased from AdooQ, MedChemExpress, and Selleckchem.

Techniques: In Vivo, Injection