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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics

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Corrections

Correction: Dual Programmed Cell Death Pathways Induced by p53 Transactivation Overcome Resistance to Oncolytic Adenovirus in Human Osteosarcoma Cells

DOI: 10.1158/1535-7163.MCT-13-0600 Published September 2013
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In this article (Mol Cancer Ther 2013;12:314–25), which appeared in the March 2013 issue of Molecular Cancer Therapeutics (1), the authors regret that the actin panel for A-p53 in Fig. 3A is incorrect. We used the same membrane for analyzing multiple protein expression and, therefore, the actin panel should be the same for different proteins, but not for different cell lines. The corresponding author apologizes for the error made during the revision process. The correct actin panel for Ad-p53 is used in the last panel of Fig. 3A. Please see the correct Fig. 3A below.

Figure 3.
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Figure 3.

OBP-702 induces p53 overexpression with E1A-mediated p21 suppression via miR-93 and miR-106b activation. A, expression of the p53 and p21 proteins in SaOS-2 and MNNG/HOS cells infected with OBP-702 or Ad-p53 at the indicated MOIs for 72 hours was assessed using Western blot analysis. B, expression of the E2F1 and viral E1A proteins in SaOS-2 and MNNG/HOS cells infected with OBP-702 at the indicated MOIs for 72 hours was assessed using Western blot analysis. C, expression of miR-93 and miR-106b was assayed using qRT-PCR in SaOS-2 cells infected with OBP-702 at the indicated MOIs for 72 hours in 3 independent experiments. The values of miR-93 and miR-106b at 0 MOI were set at 1, and the relative levels of miR-93 and miR-106b at the indicated MOIs were plotted as fold induction. Bars, SD. Statistical significance was determined by Student t test; *, P < 0.05. D, SaOS-2 cells were transfected with 10 nmol/L miR-93, miR-106, or control miRNA 24 hours before Ad-p53 infection at an MOI of 100. Forty-eight hours after Ad-p53 infection, the expression levels of p53, p21, PARP, and C-PARP were examined by Western blot analysis. β-Actin was assayed as a loading control. By using ImageJ software, the expression level of C-PARP protein was calculated relative to its expression in the control miR–treated cells, whose expression level was designated as 1.0.

  • ©2013 American Association for Cancer Research.

Reference

  1. 1.↵
    1. Hasei J,
    2. Sasaki T,
    3. Tazawa H,
    4. Osaki S,
    5. Yamakawa Y,
    6. Kunisada T,
    7. et al.
    , Dual programmed cell death pathways induced by p53 transactivation overcome resistance to oncolytic adenovirus in human osteosarcoma cells. Mol Cancer Ther 2013;12:314–25.
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Molecular Cancer Therapeutics: 12 (9)
September 2013
Volume 12, Issue 9
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Correction: Dual Programmed Cell Death Pathways Induced by p53 Transactivation Overcome Resistance to Oncolytic Adenovirus in Human Osteosarcoma Cells
Mol Cancer Ther September 1 2013 (12) (9) 1920-1921; DOI: 10.1158/1535-7163.MCT-13-0600

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Correction: Dual Programmed Cell Death Pathways Induced by p53 Transactivation Overcome Resistance to Oncolytic Adenovirus in Human Osteosarcoma Cells
Mol Cancer Ther September 1 2013 (12) (9) 1920-1921; DOI: 10.1158/1535-7163.MCT-13-0600
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Molecular Cancer Therapeutics
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