Journal: Biology Direct

Article Title: MEF2A activates the ZDHHC20/NF-κB pathway to inhibit doxorubicin sensitivity and promote the malignant progression of acute myeloid leukemia

doi: 10.1186/s13062-026-00762-y

Figure Lengend Snippet: MEF2A expression was upregulated in AML. ( A ) Analysis of MEF2A expression across pan-cancer samples. ( B ) The GEPIA database was used to analyze MEF2A expression in AML tissues and normal samples. ( C ) MEF2A mRNA expression was detected by qRT-PCR in AML samples ( N = 42) and healthy samples ( N = 16). ( D ) The western blotting assay was performed to detect MEF2A protein expression in AML samples and healthy samples. ( E ) MEF2A mRNA expression was detected by qRT-PCR in HS-5, HL-60, MOLM-13, THP-1, U937, and KG-1 cells. ( F ) MEF2A protein expression was analyzed by western blotting assay in HS-5 cells, HL-60 cells, and KG-1 cells

Article Snippet: AML cell lines (MOLM-13, THP-1, and U937, Procell, Wuhan, China) were cultured in RPMI-1640 added with 10% fetal bovine serum (EK-Bioscience) and 1% penicillin/streptomycin (Millipore) at 37°C with 5% CO 2 .

Techniques: Expressing, Quantitative RT-PCR, Western Blot

Journal: Cell reports

Article Title: Retinoic acid and ascorbate synergize to suppress myeloid leukemia via TET2 activation

doi: 10.1016/j.celrep.2025.116379

Figure Lengend Snippet: (A) Correlation matrix of genes with significant ( p < 0.05) Pearson’s R value. Genes highlighted in red represent genes of interest with positive correlations. Color and size of dots are scaled to the R value and absolute R value, respectively. (B) Correlation plots of RARA expression vs. TET1–3 expression in AML patient samples using publicly available BeatAML dataset. (C) TET2 expression changes upon ATRA stimulation from four different published datasets of APL cell lines. (D–G) Human AML cell lines measured for TET and RAR mRNA levels following 3 days of treatment with 1 μM ATRA. (D) Fold change of TET1–3 mRNA levels upon ATRA stimulation. (E and F) Basal expression of TET (E) and RAR (F) genes across AML lines. Mean ± SEM, n = 2–3. (G) TET1–3 mRNA levels in select AML cell lines treated with ATRA sampled over 72 h. Mean ± SEM, n = 3. (H and I) Fold change of TET1–3 mRNA in response to RAR agonists—retinol, tamibarotene, and ATRA—(H) or RARA-antagonist treatment ± ATRA (I) for 3 days in U-937 cells. Mean ± SEM, Student’s paired t test, n = 3. (J) (Top) RARE motif within the TET2 locus. (Bottom) Anti-RARA ChIP-qPCR of canonical retinoic acid responsive element ( RARE ) regions upon 3-day ATRA treatment in MV4–11 and U-937 cells. A region with no RARE motif (non- RARE ) at exon 11 of the TET2 gene was used as a negative control. Mean ± SEM, Student’s t test, n = 2. (K and L) Basal RARA expression (K) and fold change of TET1–3 expression (L) with ATRA stimulation upon CRISPR knockdown of RARA (single guide [sg] RARA ) in MV4–11 and U-937 cells, compared to non-targeting guide (NTG) controls. Mean ± SEM, n = 3. Two-way ANOVA. * p < 0.05, ** p < 0.005, *** p < 0.0005, and **** p < 0.00005.

Article Snippet: For generation of CRISPER-knockdown cell lines, sg RARA AML cell lines (MV4–11 & U-937) were generated using lentiCRISPRv2 (Addgene plasmid #52961; http://n2t.net/addgene:52961 ; RRID:Addgene_52961).

Techniques: Expressing, ChIP-qPCR, Negative Control, CRISPR, Knockdown

Journal: Cell reports

Article Title: Retinoic acid and ascorbate synergize to suppress myeloid leukemia via TET2 activation

doi: 10.1016/j.celrep.2025.116379

Figure Lengend Snippet: (A) Fold change (FC) of TET1–3 mRNA in KASUMI-1, MOLM-13, MV4–11, and U-937 after 1 μM ATRA treatment for 3 days. Mean ± SEM, n = 3–6. (B and C) Heatmap of ATRA IC 50 (B) and Bliss synergy scores with L-AA (C) across the AML cell lines. Mean ± SEM, n = 3–6. (D) Wright-Giemsa stains of MV4–11 and U-937 cells treated with vehicle, 250 μM L-AA, 1 μM ATRA, or the combination for 3 days. Representative of 3 experiments. (E–G) Screen of 354 cell surface markers following 3-day treatment of MV4–11 and U-937 cells with L-AA and ATRA. (E) Experimental procedure for cell trace staining and flow cytometry analysis. (F) Log 2 FC of all cell surface markers relative to vehicle for (left) MV4–11 and (right) U-937. (G) Heatmap of surface markers with ≥1.5 FC in both cell lines. (H) Relative mean fluorescence intensity (MFI) of select cell surface markers with RARA knockout (sg RARA ) vs. non-targeting guide (NTG) control MV4–11 and U-937 cells. Mean ± SEM, n = 2. (I–L) Heatmap of ATRA IC 50 (I) and Bliss synergy scores of L-AA and ATRA co-treatment (J) for 72 h and viability (K) and cell cycle analysis (L) of NTG and sgRARA AML cell lines grown for 14 days. Mean ± SEM, n = 2. Two-way ANOVA. * p < 0.05, ** p < 0.005, *** p < 0.0005, and **** p < 0.00005.

Article Snippet: For generation of CRISPER-knockdown cell lines, sg RARA AML cell lines (MV4–11 & U-937) were generated using lentiCRISPRv2 (Addgene plasmid #52961; http://n2t.net/addgene:52961 ; RRID:Addgene_52961).

Techniques: Staining, Flow Cytometry, Fluorescence, Knock-Out, Control, Cell Cycle Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Anti-inflammatory Role of Carotenoids in Endothelial Cells Derived from Umbilical Cord of Women Affected by Gestational Diabetes Mellitus

doi: 10.1155/2019/8184656

Figure Lengend Snippet: Effect of carotenoids on TNF- α -induced monocyte interaction in C- and GD-HUVECs. Monocyte-HUVEC adhesion in C- and GD-HUVECs untreated (Basal) and incubated for 24 h with BC or Lyc (2.5 μ mol/L) and then stimulated for 16 h with or without TNF- α (1 ng/mL). In the histogram (upper side), quantitative data express the number of U937 cells adhering within a high-power field (3.5mm 2 ). Each measurement is expressed as the mean ± SD of adhering cells from 3 experiments ( n = 3), each consisting of 8 counts per condition. In the lower side, representative photos of C- and GD-HUVECs for each experimental condition. ANOVA and Bonferroni multiple comparison test: ∗ p < 0.05 vs. basal C-HUVECs, ∗∗ p < 0.05 vs. TNF- α C-HUVECs, ∗∗∗ p < 0.05 vs. Basal GD-HUVECs, # p < 0.05 vs. TNF- α GD-HUVECs. Student'st-test: † p < 0.0002 basal GD-HUVECs vs. basal C-HUVECs, ‡ p < 0.0001 TNF- α GD-HUVECs vs. TNF- α C-HUVECs.

Article Snippet: The cells were grown to confluence in six-well tissue culture plates and U937 cell lines (European Collection of Authenticated Cell Cultures (ECACC)) were used to evaluate the adhesion to HUVEC monolayers as previously described [ ].

Techniques: Incubation, Comparison