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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2013 Feb 12;110(10):4147–4148. doi: 10.1073/pnas.1300338110

Correction for Gururaj et al., MTA1, a transcriptional activator of breast cancer amplified sequence 3

PMCID: PMC3593887

MEDICAL SCIENCES Correction for “MTA1, a transcriptional activator of breast cancer amplified sequence 3,” by Anupama E. Gururaj, Rajesh R. Singh, Suresh K. Rayala, Caroline Holm, Petra den Hollander, Hao Zhang, Seetharaman Balasenthil, Amjad H. Talukder, Goran Landberg, and Rakesh Kumar, which appeared in issue 17, April 25, 2006, of Proc Natl Acad Sci USA (103:6670–6675; first published April 14, 2006; 10.1073/pnas.0601989103).

The authors note the following: “We have recently become aware that errors were introduced into Figs. 1 and 2 during their composition. In Fig. 1, the control panels were reused in Fig. 1A and Fig. 1F, and the incorrect MTA1 panel was used in Fig. 1J. We have now replaced the panels with correct panels from the original experimental results. In Fig. 2, the ER panel in Fig. 2C was reused in Fig. 2H. We have now replaced the panel with the correct panel in Figure 2H. Additionally, the RT-PCR panels of Fig. 2E and 2F were originally spliced together. We have now replaced these RT-PCR panels with results from repeat experiments. These errors do not change the original scientific conclusions and validity of the result remains the same.” The corrected figures and their corresponding legends appear below.

Fig. 1.

Fig. 1.

Recruitment to the regulatory region and modulation of BCAS3 by MTA1. (A) MTA1-associated chromatin from MCF-7 cells associates with regulatory region of BCAS3. (B) Levels of BCAS3 and MTA1 in MCF-7/MTA1 (T11 clone) and MCF-7/pcDNA cells. (C) Effect of MTA1 knockdown by RNAi on the levels of BCAS3. (D) Effect of T7-MTA1 or pCDNA on the BCAS3-luc activity in MCF-7 cells. Inset, expression of transfected T7-MTA1. (E) Status of BCAS3-luc activity in MCF-7/MTA1 and HC11/MTA1 clones with respective controls. (F) Recruitment of MTA1 onto BCAS3 regulatory region upon E2 stimulation. (G) BCAS3-luc reporter activity in MCF-7 cells transiently transfected with T7-MTA1 and treated with E2. (H and I) Effect of E2 treatment on BCAS3-luc activity and BCAS3 protein in MCF-7/pcDNA and MCF-7/MTA1 cells. Luciferase activity is represented as fold induction by E2 as compared to control (n = 3). (J) Effect of MTA1 depletion on BCAS3 expression in MCF-7 cells treated with or without E2 (n = 3).

Fig. 2.

Fig. 2.

Occupancy of BCAS3 enhancer module by ERα and regulation of gene expression. (A) E2 stimulation promotes ERα recruitment onto BCAS3 regulatory region in MCF-7 cells. (B) ERα occupancy of BCAS3 regulatory sequence upon E2 treatment. (C) Effect of ERα depletion upon E2 stimulation of BCAS3-luc activity in MCF-7 cells. (D) BCAS3-luc activity in HeLa cells transfected with ERα or vector and treated with E2. (E) Effect of E2 stimulation on BCAS3 mRNA in MCF-7 cells. (F) Inhibition of E2-induced BCAS3 expression by ICI-182780 in MCF-7 cells. (G) Effect of ERα knockdown on BCAS3 expression in MCF-7 cells treated with or without E2. (H) (Right) Recruitment of MTA1 onto BCAS3 regulatory region in response to E2 stimulation in ER-depleted MCF-7 cells. (Left) Status of ERα knockdown by RNAi (n = 3).


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