Open Access

Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation

  • Mariana Toricelli1,
  • Fabiana H. M. Melo1, 2,
  • Giovani B. Peres3,
  • Débora C. P. Silva4 and
  • Miriam G. Jasiulionis1Email author
Molecular Cancer201514:161

https://doi.org/10.1186/s12943-015-0405-2

Published: 22 August 2015

The original article was published in Molecular Cancer 2013 12:1095

Erratum

After publication of this study [1], we found out that we unfortunately sent two figures in duplicate. They are Fig. 4b NT and Fig. 6c NT [1]. It is important to emphasize that the results shown in the graphs are correct since they represent the mean of three independent biological assays, each of them made in technical triplicates. The photographs are only representative figures of three biological assays.
Fig. 4

PI3-K signaling pathway is involved in anoikis resistance phenotype conferred by Timp1. The MaGFP and MaT1S cell lines were treated overnight with PI3-K inhibitors, Wortmannin (a) or LY294002 (b), and their clonogenic capability was evaluated. c Melan-a melanocytes stably transfected with GFP (control transfection, MaGFP) and Timp1 (MaT1S) were maintained in suspension for 1, 3, 5 and 24 hours. The Akt activation was assessed by Western blotting. *p < 0.05, **p < 0.01, ****p < 0.0001

Fig. 6

PI3-K inhibition renders melanoma cells anoikis sensitive. The 4C11- and 4C11+ melanoma cell lines were maintained in suspension for 96 hours in the presence of Wortmannin (a and b, respectively) or LY294002 (c and d, respectively). After 96 hours, suspended cells were plated and after 5 days clonogenic capacity was analyzed. 4C11-: non-metastatic melanoma cells; 4C11+: metastatic melanoma cells; NT: non-treated; Wn: Wortmannin; LY: LY294002. *p < 0.05, **p < 0.01, ***p < 0.001

Notes

Declarations

Authors’ Affiliations

(1)
Pharmacology Department, Universidade Federal de São Paulo
(2)
Microbiology, Immunology and Parasitology Department, Universidade Federal de São Paulo
(3)
Biochemistry Department, Universidade Federal de São Paulo
(4)
Ludwig Institute for Cancer Research

Reference

  1. Mariana T, Fabiana HM M, Peres GB, Débora CP S, Jasiulionis MG. Timp1 interacts with beta-1integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation. Molecular Cancer. 2013;12:22.Google Scholar

Copyright

© Toricelli et al. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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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