[Corrigendum] The pterocarpanquinone LQB-118 induces apoptosis in acute myeloid leukemia cells of distinct molecular subtypes and targets FoxO3a and FoxM1 transcription factors.

Subsequent to the publication of the above article, the authors have realized that there were errors associated with Figs. 1c and 2b. In Fig. 1c, the authors noted that the same data were incorrectly presented for the 'Untreated cells" and 'DMSO' dot­blot experiments. After having re­examined their source data, the authors were able to confirm that the data correctly shown for the 'Untreated cells' experiment had inadvertently been included in the Figure as the data for the 'DMSO' experiment. Additionally, in Fig. 2b, the authors noticed that the percentage of untreated cells with active caspase­3 was missing (the label for the 'No antibody' experiment). Corrected versions of Figs. 1 (including the correct data for the 'DMSO' dot blot) and 2 (with the label now incorporated) are shown opposite. Note that these changes do not affect the results or the conclusions reported in this paper, and all the authors agree to this correction. The authors apologize to the Editor and to the readership of the Journal for any inconvenience caused. [the original article was published in International Journal of Oncology 45: 1949­1958, 2014; DOI: 10.3892/ijo.2014.2615].

The pterocarpanquinone LQB-118 induces apoptosis in acute myeloid leukemia cells of distinct molecular subtypes and targets FoxO3a and FoxM1 transcription factors.

Acute myeloid leukemia (AML) patients' outcome is usually poor, mainly because of drug resistance phenotype. The identification of new drugs able to overcome mechanisms of chemoresistance is essential. The pterocarpanquinone LQB-118 compound has been shown to have a potent cytotoxic activity in myeloid leukemia cell lines and patient cells. Our aim was to investigate if LQB-118 is able to target FoxO3a and FoxM1 signaling pathways while sensitizing AML cell lines. LQB-118 induced apoptosis in both AML cell lines HL60 (M3 FAB subtype) and U937 (M4/M5 FAB subtype). Cell death occurred independently of alterations in cell cycle distribution. In vivo administration revealed that LQB-118 was not cytotoxic to normal bone marrow-derived cells isolated from mice. LQB-118 induced FoxO3a nuclear translocation and upregulation of its direct transcriptional target Bim, in HL60 cells. However, LQB-118 induced FoxO3a nuclear exclusion, followed by Bim downregulation, in U937 cells. Concomitantly, LQB-118 exposure reduced FoxM1 and Survivin expression in U937 cells, but this effect was more subtle in HL60 cells. Taken together, our data suggest that LQB-118 has a selective and potent antitumor activity against AML cells with distinct molecular subtypes, and it involves differential modulation of the signaling pathways associated with FoxO3a and FoxM1 transcription factors.