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Erschienen in: Cancer Cell International 1/2015

Open Access 01.12.2015 | Erratum

Erratum to: PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells

verfasst von: Lei Qi, Hidemi Toyoda, Dong-qing Xu, Ye Zhou, Naoto Sakurai, Keishirou Amano, Kentaro Kihira, Hiroki Hori, Eiichi Azuma, Yoshihiro Komada

Erschienen in: Cancer Cell International | Ausgabe 1/2015

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The online version of the original article can be found under doi:10.​1186/​s12935-015-0239-4.
The online version of the original article can be found at http://​dx.​doi.​org/​10.​1186/​s12935-015-0239-4.

Erratum to: Cancer Cell Int (2015) 15:91 DOI 10.1186/s12935-015-0239-4

Unfortunately, the original version of this article [1] contained an error. After publication it came to the authors’ attention that the figure legends were displayed incorrectly. The correct figure legends can be found below in this erratum.
Fig. 1 MK-2206 suppressed the cell growth of NB cells. a MK-2206 suppressed the cell growth of NB cell lines. LAN-1, KP-N-SIFA, NB-19, and SK-N-DZ cells were cultured in RPMI1640 + 10 % FBS with MK-2206 at indicated concentrations. Cell growth was evaluated as cell numbers at 72 h, and it was repeated three times. Data are expressed as the mean (±SD). b Photomicrographs of MK-2206 non-resistant and resistant cells. Cells were cultured in glass bottom slide chambers with RPMI1640 + 10 % FBS, with MK-2206 (resistant sublines)/without MK-2206 (non-resistant cells) overnight. A 50 µm scale is indicated (Olympus Fluoview fv1000, DIC acquisition, ×40). c MK-2206 showed less inhibition in the proliferation of MK-2206-resistant sublines than in the non-resistant cells. Indicated cells were cultured in RPMI1640 + 10 % FBS with MK-2206 at indicated concentrations. Cell growth was evaluated as cell numbers at indicated hours, and it was repeated three times. Data are expressed as the mean (±SD). *P < 0.01
Fig. 2 MK-2206 showed less inhibition in cell growth of MK-2206-resistant sublines. a MK2206 suppressed cell growth in a dose dependent method, and MK-2206-resistant sublines maintained resistance after 2-week withdrawal of MK-2206. Indicated cells were cultured in RPMI1640 + 10 % FBS with MK-2206 at the indicated concentrations. Cell growth was evaluated as cell numbers at 72 h, and it was repeated three times. Data are expressed as the mean (±SD). b IC50 of MK-2206 in indicated cells. c The effect of MK-2206 on cell cycle phase distribution. LAN-1 and LAN-1-MK were treated with/without MK-2206 (5 µM) in RPMI1640 with 10 % FBS for 12 h followed by analysis of cell cycle phase distribution, as introduced in “Methods”. Cells were stained with propidium iodide (PI) for 30 min followed by FACScan flow cytometer. d Column chart of cell cycle distribution in c
Fig. 3 Effect of GSK2334470 (GSK), PDK1 inhibitor, in MK-2206-resistant sublines compared with non-resistant cells. a Indicated cells were treated with GSK at indicated concentrations, with/without MK-2206 (5 µM) in RPMI1640 + 10 % FBS. Cell growth was evaluated as cell numbers at 72 h, and it was repeated three times. Data are expressed as the mean (±SD). b IC50 of GSK in indicated cells. c The effect of GSK on cell cycle phase distribution in LAN-1 and LAN-MK. LAN-1 and LAN-1-MK were treated with GSK (5 µM) with/without MK-2206 (5 µM) in RPMI1640 with 10 % FBS for 12 h followed by analysis of cell cycle phase distribution, as introduced in “Methods”. Indicated cells were stained with PI for 30 min followed by FACScan flow cytometer
Fig. 4 Effect of AZD8055 (AZD), mTOR inhibitor, in MK2206 resistant sublines compared with non-resistant cells. a Indicated cells were treated with AZD at indicated concentrations, with/without MK-2206 (5 µM) in RPMI1640 + 10 % FBS. Cell growth was evaluated as cell numbers at 72 h, and it was repeated three times. Data are expressed as the mean (±SD). b IC50 of AZD in indicated cells. c The effect of AZD on cell cycle phase distribution in LAN-1 and LAN-MK. LAN-1 and LAN-1-MK were treated with AZD (50 nM) with/without MK-2206 (5 µM) in RPMI1640 with 10 % FBS for 12 h followed by analysis of cell cycle phase distribution, as introduced in “Methods”. Indicated cells were stained with PI for 30 min followed by FACScan flow cytometer
Fig. 5 Effect of GSK2334470 (GSK) on PDK1-mTOR-S6K axis in MK-2206-resistant sublines. ad After 1 h serum starvation, indicated cells were incubated in RPMI1640 + 10 % FBS with/without MK-2206 (5 µM) or GSK (5 µM). Phosphorylation of PDK1, AKT, mTOR, and S6K were detected by western blot at 1.5 and 12 h, so were AKT and Actin. GSK3β, p-GSK3β and N-MYC were also detected
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://​creativecommons.​org/​licenses/​by/​4.​0/​), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://​creativecommons.​org/​publicdomain/​zero/​1.​0/​) applies to the data made available in this article, unless otherwise stated.
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1.
Zurück zum Zitat Qi L, Toyoda H, Xu D, Zhou Y, Sakurai N, Amano K, Kihira K, Hori H, Azuma E, Komada Y, et al. PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells. Cancer Cell International. 2015;15:91.PubMedCentralCrossRefPubMed Qi L, Toyoda H, Xu D, Zhou Y, Sakurai N, Amano K, Kihira K, Hori H, Azuma E, Komada Y, et al. PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells. Cancer Cell International. 2015;15:91.PubMedCentralCrossRefPubMed
Metadaten
Titel
Erratum to: PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells
verfasst von
Lei Qi
Hidemi Toyoda
Dong-qing Xu
Ye Zhou
Naoto Sakurai
Keishirou Amano
Kentaro Kihira
Hiroki Hori
Eiichi Azuma
Yoshihiro Komada
Publikationsdatum
01.12.2015
Verlag
BioMed Central
Erschienen in
Cancer Cell International / Ausgabe 1/2015
Elektronische ISSN: 1475-2867
DOI
https://doi.org/10.1186/s12935-015-0261-6

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