Review

aml cell lines hl 60 (ATCC)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC aml cell lines hl 60

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 <t>HL-60,</t> 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.

Aml Cell Lines Hl 60, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 6533 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cells+ccl+240/HL-60/pmc13254865-332-0-13
Average 99 stars, based on 6533 article reviews

aml cell lines hl 60 - by Bioz Stars, 2026-10

99/100 stars

Images

1) Product Images from "ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance"

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

Journal: iScience

doi: 10.1016/j.isci.2026.116202

Figure Legend 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.

Techniques Used: Expressing, Mutagenesis, Two Tailed Test, Comparison

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.

Figure Legend 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.

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

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.

Figure Legend 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.

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

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.

Figure Legend 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.

Techniques Used: Control, In Vivo

Modification:

Article Title: Uremic serum damages endothelium by provoking excessive neutrophil extracellular trap formation
Article Snippet: .. HL-60 cells (CCL-240, ATCC) were maintained in Iscove’s modified Dulbecco’s medium (12440053, IMDM, Thermo Fisher Scientific) with 20% fetal bovine serum (FBS; 97068-85, VWR, Vienna, Austria). .. To differentiate HL-60 cells into neutrophil-like cells, the cells were incubated in culture medium containing 1 μM all–trans-retinoic acid (ATRA; R2625, Sigma-Aldrich) dissolved in dimethyl sulfoxide (DMSO; D2650, Sigma-Aldrich).

Article Title: Auto-amplification and spatial propagation of neutrophil extracellular traps
Article Snippet: .. HL-60 cells (CCL-240, ATCC) were cultured in Iscove’s Modified Dulbecco’s Medium (IMDM, Gibco) with 20% (v/v) heat-inactivated fetal bovine serum (FBS, Gibco) and 1% (v/v) penicillin at 37 °C in 5% \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${{CO}}_{2}$$\end{document} C O 2 . .. These cells were differentiated into neutrophil-like cells (dHL-60) by culturing with 1.3% (v/v) DMSO (Thermo Scientific) for 5 days.

Article Title: Auto-amplification and Spatial Propagation of Neutrophil Extracellular Traps
Article Snippet: .. HL-60 cells (CCL-240, ATCC) were cultured in Iscove's Modified Dulbecco's Medium (IMDM, Gibco) with 20% (v/v) heat-inactivated fetal bovine serum (FBS, Gibco) and1% (v/v) penicillin at 37°C in 5% CO!. .. These cells were differentiated into neutrophil-like cells (dHL-60) by culturing with 1.3% (v/v) DMSO (Thermo Scientific) for 5 days.

Cell Culture:

Article Title: Metabolic plasticity enables Clostridioides difficile growth in coculture with neutrophils and other mammalian cells.
Article Snippet: Objectives: Clostridioides difficile infection (CDI) is a significant healthcare burden, characterized by severe colitis and high recurrence rates.. Although neutrophils migrate rapidly to the colon infected with C. difficile, it does not lead to pathogen clearance.. Understanding how pathogen survives within the host remains a knowledge gap.

Image Search Results

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.

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.

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.

Techniques: Control, In Vivo

IC 50 Values at 24 and 48 h for HL60, A549, H2052, and HT29 Cancer Cell Lines and for the HuDe Healthy Cell Line

Journal: ACS Omega

Article Title: Multimodal Mechanism of Antitumoral Ni(II) Thiosemicarbazones: Deep Mechanistic Understanding of ROS Dynamics, Albumin-Mediated Delivery, and DNA Targeting

doi: 10.1021/acsomega.5c12067

Figure Lengend Snippet: IC 50 Values at 24 and 48 h for HL60, A549, H2052, and HT29 Cancer Cell Lines and for the HuDe Healthy Cell Line

Article Snippet: Cell lines used for biological experiments were adenocarcinomic human alveolar basal epithelial cells A549, the human acute promyelocytic leukemia cell line HL60, the human colorectal adenocarcinoma cell line HT29, and the human epithelial mesothelioma cell line H2052 (ATCC, Rockville, Maryland, United States), using non-neoplastic human dermal fibroblast cell line HuDe (Istituto Zooprofilattico Sperimentale della Lombardia e dell’Emilia (IZSLE), Brescia, Italy) for selectivity analysis.

Techniques:

Review

aml cell lines hl 60 (ATCC)

Structured Review

Images

1) Product Images from "ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance"

Related Articles

Modification:

Cell Culture:

Similar Products

Image Search Results