A3
Cat.No.: CSC-C9153W
Species: Homo sapiens (Human)
Source: Blood; Peripheral Blood
Morphology: lymphoblast
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The A3 cell line is a human T-lymphoblast subclone derived from the well-established Jurkat acute T-cell leukemia line. It was generated by treating parental Jurkat cells with Fas antibody followed by limiting dilution cloning. A key biological feature of the A3 clone is its markedly heightened sensitivity to Fas (CD95/Apo-1)-mediated apoptosis compared with the parent line, and a very low spontaneous resistance rate, making it a refined model for death receptor signaling studies.
Morphologically, A3 cells appear as round lymphoblasts and grow in suspension. They express T-cell markers including CD3 and TCR complex components. The cells are routinely cultured in RPMI-1640 medium supplemented with serum and L-glutamine, under standard conditions (37°C, 5% CO₂), and are passaged by gentle pipetting and dilution (typically 1:2 to 1:4) when the density reaches ~0.5-1 × 10⁶ cells/mL.
A3 cells are primarily used to investigate T-cell receptor (TCR) signal transduction, Fas/CD95 apoptotic pathways, NF-κB and NFAT activation, and for in vitro screening of immunomodulatory or anti-leukemic compounds.
The CDK7 Inhibitor BS-181 Induces Mitochondrial Apoptosis Primarily via the Extrinsic Pathway in T-ALL
Chemotherapy resistance in T-cell acute lymphoblastic leukemia (T-ALL) results in poor prognosis. Park et al. elucidates the mechanism of the CDK7 inhibitor BS-181 using malignant cell lines (Jurkat A3, U937, HeLa) and normal human T cells.
To determine if BS-181 induces mitochondrial apoptosis strictly via the extrinsic pathway, they compared wild-type Jurkat A3 cells with mutants deficient in key extrinsic mediators: I2.1 (FADD-deficient) and I9.2 (caspase-8-deficient). Treatment with 5-20 µM BS-181 reduced A3 viability in a dose-dependent manner (91.7% to 30.7%), whereas I2.1 and I9.2 cells were significantly less affected (Fig. 1a).
Flow cytometry confirmed this differential sensitivity. At 15 µM BS-181, A3 cells exhibited a 47.2% sub-G1 population, 46.0% mitochondrial membrane potential (ΔΨm) loss, and 44.3% BAK activation (Fig. 2b-g). In contrast, I2.1 and I9.2 cells showed markedly lower apoptosis rates (sub-G1: 13.4% and 13.2%, respectively), reduced ΔΨm loss (14.4% and 16.0%), and diminished BAK activation (15.8% and 16.3%). Interestingly, while BS-181 did not cause G1 arrest in A3 cells, it induced cell cycle arrest in the resistant I2.1 and I9.2 mutants. These results demonstrate that BS-181 primarily triggers BAK-dependent mitochondrial apoptosis as a downstream consequence of extrinsic pathway activation. However, at higher concentrations (≥15 µM), BS-181 can also bypass the requirement for FADD and caspase-8 to induce apoptosis independently.
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