human aml cell line u937  (ATCC)

Journal: iScience

Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

doi: 10.1016/j.isci.2026.116202

Figure Lengend Snippet: Expression of ALDH3A2 in healthy people and patients with AML (A) The expression of ALDH3A2 in various tumors compared with normal tissues. Data are represented as mean ± SEM. (B) Expression of ALDH3A2 in 88 leukemia cell lines. (C) The survival curve of patients with high and low expression of ALDH3A2 (n [low expression] = 121, n [high expression] = 30). (D) The expression of protein ALDH3A2 in HL-60, HL-60/ADM, K562, K562/ADM, and bone marrow in patients. (E) The expression of ALDH3A2 RNA in bone marrow mononuclear cells of AML patients in the CR ( n = 9), C1NR ( n = 8), and R/R ( n = 10) group. Data are represented as mean ± SEM. (F) The expression of ALDH3A2 in bone marrow mononuclear cells of 3 AML patients at their initial and recurrent stage. (G) High/low expression of ALDH3A2 and molecular mutation distribution of 66 AML patients. Data are represented as mean ± SEM. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

Article Snippet: AML cell lines HL-60, K562, U937, THP-1, and KG-1α were purchased from the American Type Culture Collection, while doxorubicin-resistant cell lines HL-60ADM and K562ADM were constructed by gradually increasing the concentration of Doxorubicin and inducing repeatedly over one year in HL-60 and K562.

Techniques: Expressing, Mutagenesis, Two Tailed Test, Comparison

Journal: iScience

Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

doi: 10.1016/j.isci.2026.116202

Figure Lengend Snippet: ALDH3A2-V protects AML cells from ferroptosis and cytotoxicity induced by doxorubicin (A) ALDH3A2 mRNA relative expression in HL-60/ADM and K562/ADM cells after transfection of siRNA by electroporation. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The lipid peroxidation degree of HL60ADM and K562ADM cells in the control (ctrl) and ALDH3A2 knockdown (KD) groups after the same dose of doxorubicin treatment for 48 h. (C) The content of ALDH3A2 protein in HL-60, K562, U937, and KG-1α in the ALDH3A2 overexpressing (OE) group and the control (CON) group. (D) The location of ALDH3A2-V overexpression. This representative image was selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (E) Lipid peroxidation in HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the same concentration of doxorubicin treatment. (F and G) Cell viability and its fitting curve of HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the gradient concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

Article Snippet: AML cell lines HL-60, K562, U937, THP-1, and KG-1α were purchased from the American Type Culture Collection, while doxorubicin-resistant cell lines HL-60ADM and K562ADM were constructed by gradually increasing the concentration of Doxorubicin and inducing repeatedly over one year in HL-60 and K562.

Techniques: Expressing, Transfection, Electroporation, Control, Knockdown, Over Expression, Concentration Assay, Two Tailed Test, Comparison

Journal: iScience

Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

doi: 10.1016/j.isci.2026.116202

Figure Lengend Snippet: ALDH3A2 affects the sensitivity of AML cells to doxorubicin by altering 4-HNE and fatty acid content (A) The content of 4-HNE in cell lysate and culture supernatant of AML cells in the doxorubicin treatment (ADR) group and control (CON) group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The content of 4-HNE in HL-60, U937, and KG-1α of the overexpressing ALDH3A2 (OE) group and the CON group under the same concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (C) OPLS-DA was performed on the measured fatty acids. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. (D) Variable Importance in Projection（VIP) value of different fatty acids; the difference is considered significant when the VIP>1. (E) Content of three different fatty acids in the CON and OE ALDH3A2 group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (F) Cell viability of AML cells in heptadecanoic acid, oleic acid, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (G) Lipid peroxidation in AML cells in heptadecanoic acid-, oleic acid-, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. These images were selected from 3 independent replicates. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, ∗∗ indicates p < 0.01 between the two groups, and ∗∗∗ indicates p < 0.001 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

Article Snippet: AML cell lines HL-60, K562, U937, THP-1, and KG-1α were purchased from the American Type Culture Collection, while doxorubicin-resistant cell lines HL-60ADM and K562ADM were constructed by gradually increasing the concentration of Doxorubicin and inducing repeatedly over one year in HL-60 and K562.

Techniques: Control, Concentration Assay, Two Tailed Test, Comparison

Journal: iScience

Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

doi: 10.1016/j.isci.2026.116202

Figure Lengend Snippet: X24003 inhibits ALDH3A2 and enhances the cytotoxic effects of doxorubicin on resistant AML cells (A) OPLS-DA was performed on the measured fatty acid containment in the X24003 treatment group and control group. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. VIP value of different fatty acids; the difference is considered significant when the VIP>1. (B) X24003 exhibits a synergistic effect with doxorubicin in the elimination of doxorubicin-resistant AML cell lines HL-60ADM and K562ADM. (C) X24003 augments doxorubicin-induced lipid peroxidation in doxorubicin-resistant AML cell strains without affecting the parental cell lines. The representative image was selected from three independent replicate experiments. (D) In vivo bioimaging shows the success of the model and the leukemia burden in mice before and after treatment.

Article Snippet: AML cell lines HL-60, K562, U937, THP-1, and KG-1α were purchased from the American Type Culture Collection, while doxorubicin-resistant cell lines HL-60ADM and K562ADM were constructed by gradually increasing the concentration of Doxorubicin and inducing repeatedly over one year in HL-60 and K562.

Techniques: Control, In Vivo