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International Journal of Oncology
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Print ISSN: 1019-6439 Online ISSN: 1791-2423
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August-2025 Volume 67 Issue 2

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International Journal of Molecular Medicine

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

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International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

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Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

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Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

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Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

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Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

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Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

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Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

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International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

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International Journal of Epigenetics

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Correction Open Access

[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits

  • Authors:
    • Seyung S. Chung
    • Nolan Giehl
    • Yanyuan Wu
    • Jaydutt V. Vadgama
  • View Affiliations / Copyright

    Affiliations: Division of Cancer Research and Training, Charles R. Drew University of Medicine and Science, Los Angeles, CA, USA
    Copyright: © Chung et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Article Number: 69
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    Published online on: July 14, 2025
       https://doi.org/10.3892/ijo.2025.5775
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Article

Int J Oncol 44: [Related article:] 403-411, 2014; DOI: 10.3892/ijo.2013.2195

Following the publication of the above article, a pair of interested readers drew to the Editor's attention that certain of the western blotting data featured in Figs. 1A and 3A were strikingly similar to data that had appeared in a pair of articles published previously by the same research group. Subsequently, an independent investigation of the data in this paper on the part of the Editorial Office revealed that a pair of the panels showing the results of cell invasion assays in Fig. 4A on p. 405 for the MCF7-WT cells appeared to contain overlapping sections, such that data which were intended to show results from entirely different microscopic fields had apparently been derived from partly the same original field of view.

HER2 overexpression induced pSTAT3 and
stem cell marker expression in ER-dependent manner. (A) Western
blot analyses revealed that HER2 overexpression induced pSTAT3 and
stem cell marker expression in MCF7-HER2. (B) RT-PCR confirmed that
HER2 overexpression upregulated stem cell markers of Oct-4, Sox-2
and EMT driver slug in MCF7-HER2. (C) qPCR data showed the
upregulation of CD44, vimentin, Oct-4 and Sox-2 in MCF7-HER2 cell
line. (D) Western blot analyses with down-regulation of epithelial
marker E-cadherin and upregulation of mesenchymal marker vimentin
in MCF7-HER2.

Figure 1

HER2 overexpression induced pSTAT3 and stem cell marker expression in ER-dependent manner. (A) Western blot analyses revealed that HER2 overexpression induced pSTAT3 and stem cell marker expression in MCF7-HER2. (B) RT-PCR confirmed that HER2 overexpression upregulated stem cell markers of Oct-4, Sox-2 and EMT driver slug in MCF7-HER2. (C) qPCR data showed the upregulation of CD44, vimentin, Oct-4 and Sox-2 in MCF7-HER2 cell line. (D) Western blot analyses with down-regulation of epithelial marker E-cadherin and upregulation of mesenchymal marker vimentin in MCF7-HER2.

Targeted knockdown of STAT3 gene
reduces CD44-positive cell populations. (A) shRNA driven targeted
knockdown of STAT3 gene was performed with MCF7-HER2. STAT3
knockdown was confirmed with western blot analyses. (B) FACS
profiling of CD44-positive sub-population from the control RNA and
shRNA of STAT3 in MCF7-HER2 cells are presented. (C) Western blot
analyses reaffirmed the stem cell marker abolishment upon STAT3
knockdown. (D) shRNA knockdown for HER2 gene was performed. Western
blot analyses confirmed the HER2 gene knockdown. (E) FACS profiles
of CD44-positive sub-populations from the control RNA and shRNA of
HER2 transfected cancer cells.

Figure 3

Targeted knockdown of STAT3 gene reduces CD44-positive cell populations. (A) shRNA driven targeted knockdown of STAT3 gene was performed with MCF7-HER2. STAT3 knockdown was confirmed with western blot analyses. (B) FACS profiling of CD44-positive sub-population from the control RNA and shRNA of STAT3 in MCF7-HER2 cells are presented. (C) Western blot analyses reaffirmed the stem cell marker abolishment upon STAT3 knockdown. (D) shRNA knockdown for HER2 gene was performed. Western blot analyses confirmed the HER2 gene knockdown. (E) FACS profiles of CD44-positive sub-populations from the control RNA and shRNA of HER2 transfected cancer cells.

HER2 overexpressed cells display
enhanced cell invasiveness in vitro. To measure the cell
invasiveness of MCF7 WT and MCF7-HER2, cells were subjected to
Boyden chamber assay. After 72 h of incubation, invaded cells were
monitored and counted in 2 independent areas. (A) Results of Boyden
chamber invasion assay was organized into two different microscopic
fields (×40) depicting invaded MCF7 cells. Bluish-black cells by
Toluidine blue indicate that the cell has invaded into the
matrigel. (B) Graphic representation showing increased cell
invasiveness in MCF7-HER2 cells compared to MCF7 WT cells based on
the average number of cells invaded per high powered field (HPF).
MCF7 WT averaged 8.3% invaded per HPF, while MCF7-HER2 averaged
31.3% invaded cells (p<0.05).

Figure 4

HER2 overexpressed cells display enhanced cell invasiveness in vitro. To measure the cell invasiveness of MCF7 WT and MCF7-HER2, cells were subjected to Boyden chamber assay. After 72 h of incubation, invaded cells were monitored and counted in 2 independent areas. (A) Results of Boyden chamber invasion assay was organized into two different microscopic fields (×40) depicting invaded MCF7 cells. Bluish-black cells by Toluidine blue indicate that the cell has invaded into the matrigel. (B) Graphic representation showing increased cell invasiveness in MCF7-HER2 cells compared to MCF7 WT cells based on the average number of cells invaded per high powered field (HPF). MCF7 WT averaged 8.3% invaded per HPF, while MCF7-HER2 averaged 31.3% invaded cells (p<0.05).

Upon investigating these matters with the authors, they were able to repeat the experiments concerned (in the case of Figs. 1 and 3). The revised versions of Figs. 1, 3 and 4, now featuring the replacement data for Figs. 1A and 3A and the two completely differentiated microscopic fields of view for Fig. 4, are shown on the next two pages. The authors regret that certain of the data featured in Figs. 1 and 3 of this article were erronoeusly re-used from a pair of their previous publications, and thank the Editor of International Journal of Oncology for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused.

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Copy and paste a formatted citation
Spandidos Publications style
Chung SS, Giehl N, Wu Y and Vadgama JV: [Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits. Int J Oncol 67: 69, 2025.
APA
Chung, S.S., Giehl, N., Wu, Y., & Vadgama, J.V. (2025). [Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits. International Journal of Oncology, 67, 69. https://doi.org/10.3892/ijo.2025.5775
MLA
Chung, S. S., Giehl, N., Wu, Y., Vadgama, J. V."[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits". International Journal of Oncology 67.2 (2025): 69.
Chicago
Chung, S. S., Giehl, N., Wu, Y., Vadgama, J. V."[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits". International Journal of Oncology 67, no. 2 (2025): 69. https://doi.org/10.3892/ijo.2025.5775
Copy and paste a formatted citation
x
Spandidos Publications style
Chung SS, Giehl N, Wu Y and Vadgama JV: [Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits. Int J Oncol 67: 69, 2025.
APA
Chung, S.S., Giehl, N., Wu, Y., & Vadgama, J.V. (2025). [Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits. International Journal of Oncology, 67, 69. https://doi.org/10.3892/ijo.2025.5775
MLA
Chung, S. S., Giehl, N., Wu, Y., Vadgama, J. V."[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits". International Journal of Oncology 67.2 (2025): 69.
Chicago
Chung, S. S., Giehl, N., Wu, Y., Vadgama, J. V."[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits". International Journal of Oncology 67, no. 2 (2025): 69. https://doi.org/10.3892/ijo.2025.5775
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