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. 2022 Apr 13;14(8):1955. doi: 10.3390/cancers14081955

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Resistance to PCARBTP is mediated by MDR-1, RPMI-8226-R1.0 and L-363-R3.5 are cross-resistant to PAPTP. (a,b) Parental L-363 and RPMI-8226 multiple myeloma cells and PCARBTP-resistant L-363-R3.5 and RPMI-8226-R1.0 cell lines were incubated with PCARBTP or 0.1% DMSO control in the presence or absence of elacridar as indicated. After 24 h, cell death was determined by flow cytometry with Annexin V-APC/7AAD-staining. Resistant RPMI-8226-R1.0 (c) and L-363-R3.5 cells (d) were treated with increasing concentrations PAPTP ± 100 nM elacridar for 24 h. After 24 h, cell death was determined by flow cytometry with Annexin V-APC/7AAD-staining. Values are normalized to solvent-treated control. Shown is the mean ± SD, (n = 3 independent experiments, each in duplicate).

Resistance to PCARBTP is mediated by MDR-1, RPMI-8226-R1.0 and L-363-R3.5 are cross-resistant to PAPTP. (a,b) Parental L-363 and RPMI-8226 multiple myeloma cells and PCARBTP-resistant L-363-R3.5 and RPMI-8226-R1.0 cell lines were incubated with PCARBTP or 0.1% DMSO control in the presence or absence of elacridar as indicated. After 24 h, cell death was determined by flow cytometry with Annexin V-APC/7AAD-staining. Resistant RPMI-8226-R1.0 (c) and L-363-R3.5 cells (d) were treated with increasing concentrations PAPTP ± 100 nM elacridar for 24 h. After 24 h, cell death was determined by flow cytometry with Annexin V-APC/7AAD-staining. Values are normalized to solvent-treated control. Shown is the mean ± SD, (n = 3 independent experiments, each in duplicate).