human t cell leukemia cell line  (ATCC)

Journal: Frontiers in Oncology

Article Title: Valproate reactivates HTLV-1 tax and reduces ABCB1/MDR1 expression in PBMCs derived from ATLL patients

doi: 10.3389/fonc.2026.1721313

Figure Lengend Snippet: ATLL cells from untreated patients are intrinsically resistant to topoisomerase II inhibitors. (A, B) Jurkat and ATL-2 cell lines were treated for 48 hours with increasing concentrations of DMSO, etoposide (Eto), doxorubicin (Doxo), vinblastine (VinB), oxaliplatin (OxIP), and camptothecin (CPT). (C, D) CD8 + cell–depleted PBMC were incubated for 48 hours with increasing concentrations of Eto or Doxo, respectively. Cell viability was assessed using PrestoBlue vital dye (Invitrogen), and survival rate was calculated relative to untreated controls.

Article Snippet: Human T-cell lines Jurkat (ATCC TIB-152, Manassas, VA, USA), HuT78 (ATCC TIB-161, Manassas, VA, USA), JPX9 (RRID: CVCL_0D86, BioVector NTCC, Beijing, China), HuT-102 (ATCC TIB-162, Manassas, VA, USA), C8166 (ECACC 88051601, Salisbury, UK), and ATL-2 (-) (CVCL_A6TF, RIKEN BioResource Center, Japan) were cultured in RPMI-1640 supplemented with 10% fetal calf serum (FCS) in low-binding T75 flasks (Sarstedt AG & Co, Nürmbrecht, Germany).

Techniques: Incubation

Journal: Frontiers in Oncology

Article Title: Valproate reactivates HTLV-1 tax and reduces ABCB1/MDR1 expression in PBMCs derived from ATLL patients

doi: 10.3389/fonc.2026.1721313

Figure Lengend Snippet: Expression analysis of efflux pumps from the ATP-ABC transporter family in HTLV-1-derived cell lines. (A–E) Expression of five ATP-ABC transporter family members associated with chemoresistance was assessed by RT-qPCR in two HTLV-1-negative cell lines (HuT78, Jurkat) and three HTLV-1-derived cell lines (HuT102, C81–66, ATL-2). (F, G) Relative expression of Tax and HBZ in HuT78, Jurkat, and HTLV-1-derived cell lines was measured by RT-PCR. Statistical significance was determined by one-way ANOVA with Dunn’s multiple comparisons post-test: ns, p ≤ 0.05, ** p ≤ 0.01; *** p ≤ 0.001, **** p ≤ 0.0001.

Article Snippet: Human T-cell lines Jurkat (ATCC TIB-152, Manassas, VA, USA), HuT78 (ATCC TIB-161, Manassas, VA, USA), JPX9 (RRID: CVCL_0D86, BioVector NTCC, Beijing, China), HuT-102 (ATCC TIB-162, Manassas, VA, USA), C8166 (ECACC 88051601, Salisbury, UK), and ATL-2 (-) (CVCL_A6TF, RIKEN BioResource Center, Japan) were cultured in RPMI-1640 supplemented with 10% fetal calf serum (FCS) in low-binding T75 flasks (Sarstedt AG & Co, Nürmbrecht, Germany).

Techniques: Expressing, Derivative Assay, Quantitative RT-PCR, Reverse Transcription Polymerase Chain Reaction

Journal: Frontiers in Oncology

Article Title: Valproate reactivates HTLV-1 tax and reduces ABCB1/MDR1 expression in PBMCs derived from ATLL patients

doi: 10.3389/fonc.2026.1721313

Figure Lengend Snippet: Verapamil does not inhibit ABCB1 in ATLL primary cells. (A) Western blot of unboiled extracts from control T-cell lines HuT78 (lane 1) and Jurkat (lane 2), and HTLV-1-infected lines HUT-102 (lane 3), C8166 (lane 4), ATL-2 (lane 5). IB, immunoblot. (B) Western blot of unboiled extracts from peripheral blood mononuclear cells of four HTLV-1 asymptomatic carriers (AC; lanes 1–4) and four untreated acute ATLL patients (ATL; lanes 5–8). IB, immunoblot. (C) Densitometric quantification of ABCB1 normalized to actin using ImageJ. Data are mean ± SD; significance by unpaired t-test (p = 0.0026). (D) Calcein-AM efflux assay schematic for measuring ABCB1 activity (D) in T-cell lines (E) and HTLV-1-infected PBMCs (F) . Inhibition is expressed relative to verapamil-treated controls. Data are mean ± SD; one-way ANOVA with Dunn’s multiple-comparisons post-test: ns, not significant; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

Article Snippet: Human T-cell lines Jurkat (ATCC TIB-152, Manassas, VA, USA), HuT78 (ATCC TIB-161, Manassas, VA, USA), JPX9 (RRID: CVCL_0D86, BioVector NTCC, Beijing, China), HuT-102 (ATCC TIB-162, Manassas, VA, USA), C8166 (ECACC 88051601, Salisbury, UK), and ATL-2 (-) (CVCL_A6TF, RIKEN BioResource Center, Japan) were cultured in RPMI-1640 supplemented with 10% fetal calf serum (FCS) in low-binding T75 flasks (Sarstedt AG & Co, Nürmbrecht, Germany).

Techniques: Western Blot, Control, Infection, Activity Assay, Inhibition

Journal: Frontiers in Oncology

Article Title: Valproate reactivates HTLV-1 tax and reduces ABCB1/MDR1 expression in PBMCs derived from ATLL patients

doi: 10.3389/fonc.2026.1721313

Figure Lengend Snippet: Tax inhibits ABCB1 expression in HuT78 and JPx9T-cell lines. (A) HuT78 cells were transfected with P65-Flag, P52, SP1, or Tax-Flag plasmids. Cells were harvested 48 hours post-transfection, and ABCB1 mRNA levels were measured by RT-qPCR. Statistical significance was determined by one-way ANOVA with Dunn’s multiple comparisons post-test (ns, p ≤ 0.05, * p ≤ 0.01, ** p ≤ 0.001, *** p ≤ 0.00001). (B) Western blot analysis of Tax-Flag and ABCB1 expression, with actin as the loading control. (C) Calcein-AM efflux kinetics measuring ABCB1 activity in Hut78 cells for 8 minutes with 100 µM verapamil (green curve) as a control. (D-F) JPX9 cells (human T-cell line with inducible HTLV-1 provirus) were treated for 24 hours with 20 µM cadmium chloride (CdCl2).Tax and ABCB1 expression was measured by RT-qPCR (D) and Western blotting (E, F) Inhibition of ABCB1 efflux activity was measured using the Calcein AM assay. The percentage of inhibition was calculated relative to control cells treated with verapamil.

Article Snippet: Human T-cell lines Jurkat (ATCC TIB-152, Manassas, VA, USA), HuT78 (ATCC TIB-161, Manassas, VA, USA), JPX9 (RRID: CVCL_0D86, BioVector NTCC, Beijing, China), HuT-102 (ATCC TIB-162, Manassas, VA, USA), C8166 (ECACC 88051601, Salisbury, UK), and ATL-2 (-) (CVCL_A6TF, RIKEN BioResource Center, Japan) were cultured in RPMI-1640 supplemented with 10% fetal calf serum (FCS) in low-binding T75 flasks (Sarstedt AG & Co, Nürmbrecht, Germany).

Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Control, Activity Assay, Inhibition, Calcein AM Assay

Journal: BMC Research Notes

Article Title: A genome-wide CRISPR/Cas9 screen reveals novel positive regulators of FTY720 sensitivity in acute lymphoblastic leukemia cells

doi: 10.1186/s13104-026-07654-4

Figure Lengend Snippet: Cell viabilities of Jurkat wild-type (Jurkat WT) cells and Jurkat cells stably expressing Cas9 (Jurkat-Cas9) treated with different concentrations of FTY720. (A) 24-hour and (B) 48-hour treatment timepoint. The % of cell viability was calculated in comparison to the non-treated control (Control). Data are expressed as mean ± S.D. (error bars) from 2 independent experiments. Control = non-treated control; DMSO = vehicle control

Article Snippet: Jurkat cells stably expressing Cas9 (Genecopoeia, Rockville, MD, catalog no. SL555) were grown following the manufacturer’s protocol.

Techniques: Stable Transfection, Expressing, Comparison, Control

Journal: BMC Research Notes

Article Title: A genome-wide CRISPR/Cas9 screen reveals novel positive regulators of FTY720 sensitivity in acute lymphoblastic leukemia cells

doi: 10.1186/s13104-026-07654-4

Figure Lengend Snippet: Genome-wide CRISPR/Cas9 screen for positive regulators of the FTY720 compared to DMSO (vehicle control) samples. (A) Ranking of positively selected sgRNAs of genes from the MAGeCK-VISPR analysis. The x-axis indicates the positive ranking of individual genes, and the y-axis indicates the values of the corresponding robust ranking aggregation (RRA) score. The top 10 sgRNAs of genes are highlighted and labeled. Two independent screens were performed. (B-K) The read counts (y-axis) and samples (DMSO vs . FTY720 treatment) are shown for the positively selected sgRNAs of genes (B) ZNF575 , (C) GPX3 , (D) FBXL15 , (E) DNAJB5 , (F) UBE2D1 , (G) ATXN7 , (H) C6orf201 , (I) RIC8A , (J) RAB13 and (K) C10orf12 . RRA = robust ranking aggregation score, sgRNA = single-guide RNAs

Article Snippet: Jurkat cells stably expressing Cas9 (Genecopoeia, Rockville, MD, catalog no. SL555) were grown following the manufacturer’s protocol.

Techniques: Genome Wide, CRISPR, Control, Labeling