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: Journal of oncology

Article Title: Characterization of the Newly Established Homoharringtonine- (HHT-) Resistant Cell Lines and Mechanisms of Resistance.

doi: 10.1155/2022/2813938

Figure Lengend Snippet: Figure 1: )e inhibitory effect of HHTon nine AML cell lines. (a) )e IC50 values of HHTon nine AML cell lines. (b) )e inhibitory effect of HHT on FLT3-ITD mutant cell lines was significantly higher than that in nonmutant ones. ∗P < 0.05.

Article Snippet: AML cell lines THP-1 (CVCL_0006), HL-60 (CVCL_A794), NB4 (CVCL-0005), Kasumi-1 (CVCL_0589), MOLM-13 (CVCL_2119), MV4-11 (CVCL_0064), KG-1 (CVCL_0374), and U937 (CVCL_0007) were purchased from American Type Culture Collection (ATCC), and OCI-AML3 (CVCL_1844) was purchased from Deutsche Sammlung vonMikroorganismen und Zellkulturen (DSMZ).

Techniques: Mutagenesis

Journal: Journal of oncology

Article Title: Characterization of the Newly Established Homoharringtonine- (HHT-) Resistant Cell Lines and Mechanisms of Resistance.

doi: 10.1155/2022/2813938

Figure Lengend Snippet: Figure 6: Verification of the hub genes (CALCRL and GNAI1) and the prognostic significance of CALCRL and GNAI1 for AML. (a) )e mRNA level of GPR183, CNR2, CALCRL, and GNAI1 in four AML cell lines by RT-qPCR. (b) )e protein level of CALCRL and GNAI1 in four AML cell lines and the mice tumor mass from HHT-sensitive and HHT-resistant mice groups. (c) )e expression level and OS of GNAI1 and CALCRL in online database GEPIA in AML. (d) )e OS and EFS of CALCRL in our cohorts. (e) )e correlation of GNAI1 and CALCRL through correlation analysis. P < 0.01∗∗and P < 0.001∗∗∗.

Article Snippet: AML cell lines THP-1 (CVCL_0006), HL-60 (CVCL_A794), NB4 (CVCL-0005), Kasumi-1 (CVCL_0589), MOLM-13 (CVCL_2119), MV4-11 (CVCL_0064), KG-1 (CVCL_0374), and U937 (CVCL_0007) were purchased from American Type Culture Collection (ATCC), and OCI-AML3 (CVCL_1844) was purchased from Deutsche Sammlung vonMikroorganismen und Zellkulturen (DSMZ).

Techniques: Quantitative RT-PCR, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Preclinical Evaluation of CRISPR-Edited CAR-NK-92 Cells for Off-the-Shelf Treatment of AML and B-ALL

doi: 10.3390/ijms232112828

Figure Lengend Snippet: Ligand profile characterization of leukemia cell lines. Percentage of ligand or GFP-expressing cells was determined by flow cytometry. ( a ) Ligand expression in B-ALL cell lines (KOPN-8, MHH-CALL-4, Nalm-6 and Nalm-6 GFP/Luc). ( b ) GFP expression of Nalm-6 GFP/Luc (grey) in comparison to non-transduced Nalm-6 (white). ( c ) Ligand expression in AML cell lines (NOMO-1, THP-1, U-937 and U-937 CD19tag/Luc). ( d ) CD19 expression of U-937 CD19tag/Luc (grey) in comparison to non-transduced U-937 (white).

Article Snippet: AML cell lines (NOMO-1, THP-1, U-937) and B-ALL cell lines (KOPN-8, MHH-CALL-4, Nalm-6) were obtained from the German Collection of Microorganisms and Cell Cultures GmbH (DSMZ, Braunschweig, Germany).

Techniques: Expressing, Flow Cytometry, Comparison

Journal: International Journal of Molecular Sciences

Article Title: Preclinical Evaluation of CRISPR-Edited CAR-NK-92 Cells for Off-the-Shelf Treatment of AML and B-ALL

doi: 10.3390/ijms232112828

Figure Lengend Snippet: Cytotoxicity assays in AML cell lines comparing parental NK-92 and CD276-CAR-NK-92 vs. irradiated, CBLB, NKG2A, TIGIT or triple knock-out cells. Specific lysis is shown as mean ± SD ( n = 3). Calcein assays were incubated for 2 h and several effector-to-target (E:T) ratios were employed: 10:1, 5:1, 2.5:1. Luciferase assays were studied for a time span of 6 h at 5:1 E:T ratio. ( a ) NK-92 cell lines vs. NOMO-1 calcein assay. ( b ) CD276-CAR-NK-92 cell lines vs. NOMO-1 calcein assay. ( c ) NK-92 cell lines vs. THP-1 calcein assay. ( d ) CD276-CAR-NK-92 cell lines vs. THP-1 calcein assay. ( e ) NK-92 cell lines vs. U-937 calcein assay. ( f ) CD276-CAR-NK-92 cell lines vs. U-937 calcein assay. ( g ) NK-92 cell lines vs. U-937 CD19tag/Luc luciferase assay. ( h ) CD276-CAR-NK-92 cell lines vs. U-937 CD19tag/Luc luciferase assay. * p < 0.05; ** p < 0.01; *** p > 0.001; **** p < 0.0001; ns, non-significant ( p > 0.05).

Article Snippet: AML cell lines (NOMO-1, THP-1, U-937) and B-ALL cell lines (KOPN-8, MHH-CALL-4, Nalm-6) were obtained from the German Collection of Microorganisms and Cell Cultures GmbH (DSMZ, Braunschweig, Germany).

Techniques: Irradiation, Knock-Out, Lysis, Incubation, Luciferase

Journal: Cancer Immunology Research

Article Title: Broad Cytotoxic Targeting of Acute Myeloid Leukemia by Polyclonal Delta One T Cells

doi: 10.1158/2326-6066.cir-18-0647

Figure Lengend Snippet: Figure 2. Clonal DOT-cell reactivity against AML cells. A and B, In vitro killing of AML KG-1 cells by DOT-cell clones generated from single Vd1þ T cells sorted from healthy donors. Cells were coincubated for 3 hours at 10:1 (E:T) ratio and then analyzed by Annexin V staining (percentage of positive events among prelabeled KG-1 cells). Each bar represents killing of KG-1 cells upon coincubation with individual clones. Dashed red line represents the mean basal tumor cell death (without DOT cells). In B, either anti-Vd1þ TCR-specific mAb or isotype control was added to the cultures. Shown are the clones where the blockade led to clearer reduction in KG-1 targeting. Data represent the average of two technical replicates and are derived from 4 independent healthy donors (HD). C, Real-time PCR assessing B7-H6 mRNA in parental (B7-H6þ/þ) and CRISPR/Cas9-manipulated (B7-H6/) AML HEL cell lines. D, In vitro killing of B7-H6þ/þ or B7-H6/ AML HEL cells by bulk DOT cells produced from 3 healthy donors (tested in technical duplicates). Cells were coincubated for 3 hours at 10:1 (E:T) ratio and then analyzed by Annexin V staining (shown are percentages of positive events among prelabeled HEL cells). Indicated are mean þ SEM (, P < 0.001).

Article Snippet: AML cell targeting in vitro and in vivo AML cell lines (THP-1, HEL, AML-193, MV4-11, HL-60, U-937, OCI-AML3, Kasumi-1, and KG-1) were obtained from and authenticated by the German Resource Center for Biologic Mate- rial (DSMZ); and used at passages p3–p8.

Techniques: In Vitro, Clone Assay, Generated, Staining, Control, Derivative Assay, Real-time Polymerase Chain Reaction, CRISPR, Produced

Journal: Cancer Immunology Research

Article Title: Broad Cytotoxic Targeting of Acute Myeloid Leukemia by Polyclonal Delta One T Cells

doi: 10.1158/2326-6066.cir-18-0647

Figure Lengend Snippet: Figure 3. DOT cells target multiple AML cell types but not healthy leukocytes. In vitro killing assays with DOT cells produced from 3–4 healthy donors, coincubated for 3 hours at 10:1 (E:T) ratio with the indicated AML cell lines (A), primary AML samples (B), or normal leukocyte populations FACS-sorted from the peripheral blood (C). In A, the dashed red line represents the mean basal tumor cell death; and in B, CTR refers also to tumor cells alone (without DOT cells). Experiments were performed with technical triplicates. In vivo AML targeting by DOT cells. DOT cells (3 injections of 2 107 cells, see Supplementary Fig. S5A–S5C) were transferred to NSG mice (n ¼ 6 CTR, 7 DOT-treated mice) preinjected with KG-1 AML cells (D–E); or NSGS mice (n ¼ 5 CTR, 5 DOT-treated mice) bearing primary AML cells (F–G; patient-derived xenograft, PDX). Tumor burden was assessed in the blood and liver one week after the last DOT-cell transfer (D); or through weekly bleedings (F). Indicated are mean þ SEM, , P < 0.05; , P < 0.001; , P < 0.0001. Animals were sacrificed when advanced disease symptoms (such as back leg paralysis) were observed. Survival curves are presented in panels E (P < 0.05) and G (P < 0.01).

Article Snippet: AML cell targeting in vitro and in vivo AML cell lines (THP-1, HEL, AML-193, MV4-11, HL-60, U-937, OCI-AML3, Kasumi-1, and KG-1) were obtained from and authenticated by the German Resource Center for Biologic Mate- rial (DSMZ); and used at passages p3–p8.

Techniques: In Vitro, Produced, In Vivo, Derivative Assay

Journal: Cancer Immunology Research

Article Title: Broad Cytotoxic Targeting of Acute Myeloid Leukemia by Polyclonal Delta One T Cells

doi: 10.1158/2326-6066.cir-18-0647

Figure Lengend Snippet: Figure 4. DOT cells (re-)target chemotherapy-resistant AML. Comparison of the in vitro anti-AML activity of DOT cells and standard chemotherapy. A, DOT cells and standard AML chemotherapy (doxorubicin plus cytarabine) protocols were tested against chemotherapy-na€ve (wild type, wt) or chemo-relapsed (CR, regrown after >99% HEL cell elimination) AML cells. Shown are the percentages of Annexin Vþ HEL cells after 3 hours of treatment. B, Number of AML HEL cells before and after 72 hours of treatment with DOT cells (at 5:1 E:T ratio). Surviving cells (<1%) were resorted and allowed to regrow, thus generating the DOT-treated (DT) samples of (C–E). C, DOT cells were coincubated for 3 hours with nontreated (NT) or previously DOT-treated (DT) AML HEL cells at 5:1 or 10:1 (E:T) ratios. Shown are the percentages of Annexin Vþ HEL cells. D, Number of barcoded AML single-cell lineages in non-treated (NT), chemotherapy-treated (CT), or DOT-treated (DT) AML HEL cells. E, Pearson correlation for distribution of barcoded AML single-cell lineages between different treatments. Red, yellow, and green dashed lines represent low, medium, and high correlations, respectively. Indicated are mean þ SEM (, P < 0.01; , P < 0.001; , P < 0.0001).

Article Snippet: AML cell targeting in vitro and in vivo AML cell lines (THP-1, HEL, AML-193, MV4-11, HL-60, U-937, OCI-AML3, Kasumi-1, and KG-1) were obtained from and authenticated by the German Resource Center for Biologic Mate- rial (DSMZ); and used at passages p3–p8.

Techniques: Comparison, In Vitro, Activity Assay, Single Cell