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

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 inhibitors enhance oxaliplatin efficacy in colorectal cancer with RB-dependent and tumor-selective activity in intestinal model

doi: 10.64898/2026.04.15.718743

Figure Lengend Snippet: HCT116 cells (5 × 10³ cells/well) were exposed for 48 h to increasing concentrations of (A) 5-fluorouracil (0.77–7700 μM), (B) SN-38 (0.02–200 nM), (C) oxaliplatin (0.125–250 μM), and (D) the CDK4/6 inhibitors abemaciclib (25–3000 nM) or palbociclib (25–6400 nM). Cell viability was assessed by Calcein AM fluorescence and expressed as a percentage of the untreated control (100%). The data are presented as the mean ± SEM of six independent biological replicates. Dose–response curves were fitted by nonlinear regression using a four-parameter logistic model (variable slope; log[inhibitor] vs. normalized response) in GraphPad Prism 8.4.3.

Article Snippet: The selective CDK4/6 inhibitors abemaciclib (MedChemExpress, HY-16297A) and palbociclib (MedChemExpress, HY-A0065) were used either as single agents or in combination with one of the following chemotherapeutic agents: 5-fluorouracil (5-FU; Merck, F6627), SN-38 (7-ethyl-10-hydroxycamptothecin; Cayman Chemical, 15632), and oxaliplatin (Bergamo, 1151955).

Techniques: Fluorescence, Control

Journal: bioRxiv

Article Title: CDK4/6 inhibitors enhance oxaliplatin efficacy in colorectal cancer with RB-dependent and tumor-selective activity in intestinal model

doi: 10.64898/2026.04.15.718743

Figure Lengend Snippet: HCT116 cells were treated with increasing concentrations of chemotherapeutic agents in the absence or presence of fixed concentrations of CDK4/6 inhibitors, and cell viability was assessed by Calcein AM fluorescence and expressed as a percentage relative to the untreated control (100%). (A) 5-fluorouracil, (B) SN-38, (C) oxaliplatin, all of them alone or in combination with abemaciclib (300 nM). (D) Combination index (CI) analysis plotted as fraction affected versus CI for each drug combination with abemaciclib. The dashed line indicates CI = 1, where values <1 indicate synergism and values >1 indicate antagonism. (E) 5-fluorouracil, (F) SN-38, or (G) oxaliplatin, all of them alone or in combination with palbociclib (400 nM). (H) Combination index analysis plotted as fraction affected versus CI for each drug combination with palbociclib. Data are presented as mean ± SEM of at least three independent biological replicates. Bars are color-coded as follows: control (gray), chemotherapy alone (blue), abemaciclib alone (yellow), palbociclib alone (red), chemotherapy + abemaciclib (green), and chemotherapy + palbociclib (purple). Statistical significance was evaluated using ordinary one-way ANOVA followed by Šídák’s multiple comparisons test. Significance levels are indicated as follows: *p < 0.05, **p < 0.01, ***p < 0.001, ***p < 0.0001. To improve visual clarity, statistical comparisons between chemotherapy treatments alone (blue bars) and the untreated control (gray bar) are not shown in the graphs but are summarized here. ABE arm: A: CTL vs ABE ***p=0.0001; 5-FU 2.8 vs 2.8+ABE ***p=0.0005; 4.5 vs 4.5+ABE *p=0.0128; 6 vs 6+ABE ns. B: CTL vs ABE ****p<0.0001; SN-38 0.8 vs 0.8+ABE ***p=0.0009; 1.2 vs 1.2+ABE ***p=0.0004; 1.6 vs 1.6+ABE ns. C: CTL vs ABE ****p<0.0001; OXA 0.4 vs 0.4+ABE ****p<0.0001; 0.6 vs 0.6+ABE ****p<0.0001; 0.8 vs 0.8+ABE ns. PALB arm: E: CTL vs PALB ns; 5-FU 2.8 vs 2.8+PALB ns; PALB vs 2.8+PALB **p=0.0040; PALB vs 4.5+PALB ****p<0.0001; PALB vs 6+PALB ****p<0.0001; 6 vs 6+PALB *p=0.0463. F: CTL vs PALB **p=0.0071; SN-38 1.2 vs 1.2+PALB ***p=0.0008; 0.8 vs 0.8+PALB ns; 1.6 vs 1.6+PALB ns; PALB vs 1.2+PALB ***p=0.0002; PALB vs 1.6+PALB ***p=0.0003. G: CTL vs PALB *p=0.0478; OXA 0.4 vs 0.4+PALB ***p=0.0007; 0.6 vs 0.6+PALB ****p<0.0001; 0.8 vs 0.8+PALB **p=0.0041; PALB vs all OXA+PALB ****p<0.0001.

Article Snippet: The selective CDK4/6 inhibitors abemaciclib (MedChemExpress, HY-16297A) and palbociclib (MedChemExpress, HY-A0065) were used either as single agents or in combination with one of the following chemotherapeutic agents: 5-fluorouracil (5-FU; Merck, F6627), SN-38 (7-ethyl-10-hydroxycamptothecin; Cayman Chemical, 15632), and oxaliplatin (Bergamo, 1151955).

Techniques: Fluorescence, Control