Figure 7.
Glutamine transport inhibition impairs CLL metabolism and VEN resistance. (A-C) CLL cells were stimulated by CD40 (n = 4) or BCR (n = 3) for 24 hours in the presence or absence of V9302, an inhibitor of the glutamine transporter ASCT2. CLL cells were harvested, and MitoStress tests were performed on Seahorse XF analyzer. Basal and maximal OCR were measured, and spare respiration capacity and ATP-linked respiration were calculated and plotted, as was basal ECAR. (D) CD40- or BCR-stimulated CLL cells in absence/presence of V9302 (both n = 6) were collected and incubated with various concentrations of the Bcl-2 inhibitor VEN for 24 hours; cells were then stained by DioC6/TO-PRO-3 for viability measurement. Statistical analyses were performed with paired Student t test. *P < .05, **P < .01, ***P < .001. ns, not significant; UN, unstimulated control.

Glutamine transport inhibition impairs CLL metabolism and VEN resistance. (A-C) CLL cells were stimulated by CD40 (n = 4) or BCR (n = 3) for 24 hours in the presence or absence of V9302, an inhibitor of the glutamine transporter ASCT2. CLL cells were harvested, and MitoStress tests were performed on Seahorse XF analyzer. Basal and maximal OCR were measured, and spare respiration capacity and ATP-linked respiration were calculated and plotted, as was basal ECAR. (D) CD40- or BCR-stimulated CLL cells in absence/presence of V9302 (both n = 6) were collected and incubated with various concentrations of the Bcl-2 inhibitor VEN for 24 hours; cells were then stained by DioC6/TO-PRO-3 for viability measurement. Statistical analyses were performed with paired Student t test. *P < .05, **P < .01, ***P < .001. ns, not significant; UN, unstimulated control.

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