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Correction

Correction: Mitochondrial Dysfunction Promotes Breast Cancer Cell Migration and Invasion through HIF1α Accumulation via Increased Production of Reactive Oxygen Species

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Figures 3 and 6 are incorrect. The authors have provided a corrected version of each figure here.

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Figure 3. The migration capacity of subclones and their parental cells was measured by wound healing assay.

A–B, The subclones migrated faster than the parental cells SKBR3 cells (A) and 4T1 cells (B). NAC was able to effectively inhibit the migration of the subclones.

https://doi.org/10.1371/journal.pone.0114346.g001

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Figure 6. ROS promoted aggressive cellular behaviors by up-regulating HIF-1α expression.

A, The sequence of inserts in the shRNA vector clone. B, Cells with HIF-1α shRNA showed decreased HIF-1α expression compared with the control. C, Cells with HIF-1α shRNA showed decreased migration ability compared with the control as documented by transwell migration assay. **P<0.05 vs A clone (n  =  3) D, Cells with HIF-1α shRNA showed decreased invasive capacity compared with the control as documented by transwell invasion assay. **P<0.05 vs A clone (n  =  3) E, Wound healing assay showed that cells with HIF-1α shRNA migrated slower than the control.

https://doi.org/10.1371/journal.pone.0114346.g002

Reference

  1. 1. Ma J, Zhang Q, Chen S, Fang B, Yang Q, et al. (2013) Mitochondrial Dysfunction Promotes Breast Cancer Cell Migration and Invasion through HIF1α Accumulation via Increased Production of Reactive Oxygen Species. PLoS ONE 8(7): e69485

Citation: The PLOS ONE Staff (2014) Correction: Mitochondrial Dysfunction Promotes Breast Cancer Cell Migration and Invasion through HIF1α Accumulation via Increased Production of Reactive Oxygen Species. PLoS ONE 9(11): e114346. https://doi.org/10.1371/journal.pone.0114346

Published: November 25, 2014

Copyright: © 2014 The PLOS ONE Staff. 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.