AT101 treated cells demonstrate a concentration- and time-dependent decrease in viability (A, B). AT101 treatment causes concentration-dependent cytotoxicity in ST88–14 cells (C). The loss of cell viability is not accompanied by increased caspase-3 like enzymatic activity (D) and broad caspase inhibition with BAF did not protect from AT101-induced cell death (E). AT101 (15 μM for 24 hours) treatment does not increase annexin V staining in T265–2c cells (F). Staurosporine (STS) was used as a positive control for induction of caspase-3 like activity, annexin V staining and caspase-dependent apoptosis. * p-value <0.05. # = Not significant, p-value >0.05.
Treatment with AT101 leads to a concentration-dependent increase in steady state levels of LC3-II in MPNST cells (A) and a punctate LC3-like immunostaining pattern indicative of AV accumulation (B). AT101 causes an increase in autophagic flux in MPNST cells as evidenced by increased LC3 II levels in cells treated with both AT101 (10 μM for 24 hours) and BafA1 (100 nM, added 4 hours before collection of lysates) compared to either drug alone (C). T265–2c cells treated with 3-Methyladenine (3 MA–5 mM one hour prior to treatment with AT101) showed decreased level of LC3-II accumulation (D) and a modest but statistically attenuation of AT101 (15 μM for 24 hours)-induced cell death (E). Scale bar = 20 microns. * p-value <0.05.
Citation: Kaza N, Kohli L, Graham CD, Klocke BJ, Carroll SL, Roth KA (2015) Correction: BNIP3 Regulates AT101 [(-)-Gossypol] Induced Death in Malignant Peripheral Nerve Sheath Tumor Cells. PLoS ONE 10(8): e0137153. https://doi.org/10.1371/journal.pone.0137153
Published: August 27, 2015
Copyright: © 2015 Kaza et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited