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Oncology Letters
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Print ISSN: 1792-1074 Online ISSN: 1792-1082
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October-2026 Volume 32 Issue 4

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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.

International Journal of Oncology

International Journal of Oncology

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

Molecular Medicine Reports

Molecular Medicine Reports

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

Oncology Reports

Oncology Reports

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.

Oncology Letters

Oncology Letters

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

Biomedical Reports

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

Molecular and Clinical Oncology

Molecular and Clinical Oncology

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

World Academy of Sciences Journal

World Academy of Sciences Journal

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

International Journal of Functional Nutrition

International Journal of Functional Nutrition

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

International Journal of Epigenetics

International Journal of Epigenetics

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Correction Open Access

[Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis

  • Authors:
    • Ning Zhou
    • Zhongzhou Si
    • Ting Li
    • Guangshun Chen
    • Zhongqiang Zhang
    • Haizhi Qi
  • View Affiliations / Copyright

    Affiliations: Department of Organ Transplantation and General Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Article Number: 477
    |
    Published online on: August 26, 2026
       https://doi.org/10.3892/ol.2026.15832
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Article

Oncol Lett 12: [Related article:] 132–138, 2016; DOI: 10.3892/ol.2016.4580

Subsequently to the publication of the above paper, an interested reader drew the authors' attention to the fact that, regarding the cell migration assay experiments shown in Fig. 4A on p. 136, the “Negative control” data panels for the HepG2 and the HuH7 cell lines contained an overlapping section of data, suggesting that these data had been incorporated into this figure incorrectly.

CCAT2 promotes HCC cell migration. (A)
HepG2 and HuH7 cells transfected with CCAT2 shRNA or negative
control. The suppression of CCAT2 expression significantly reduced
the migration rate of the HCC cell lines when compared to the
control. (B) HepG2 and HuH7 cells transfected with
CCAT2-pcDNA3.1(+) vector or pcDNA3.1(+) empty vector.
Overexpression of CCAT2 significantly increased the migration rate
of the HCC cell lines when compared to the control. Values are
expressed as the mean ± standard deviation. Each experiment was
repeated three times. *P<0.05.

Figure 4.

CCAT2 promotes HCC cell migration. (A) HepG2 and HuH7 cells transfected with CCAT2 shRNA or negative control. The suppression of CCAT2 expression significantly reduced the migration rate of the HCC cell lines when compared to the control. (B) HepG2 and HuH7 cells transfected with CCAT2-pcDNA3.1(+) vector or pcDNA3.1(+) empty vector. Overexpression of CCAT2 significantly increased the migration rate of the HCC cell lines when compared to the control. Values are expressed as the mean ± standard deviation. Each experiment was repeated three times. *P<0.05.

Upon investigating their original data, the authors have realized that the microscopic image representing the negative control group for the HuH7 cell line was included in Fig. 4A in error. The data in this panel have been replaced with correct data for the negative control group for the HuH7 cell line, and the accompanying statistical analyses have been rectified accordingly. The revised version of Fig. 4 is shown on the next page. It is important to note that the replacement of the data in this figure has not significantly changed either the results or the conclusions reported in this study.

All the authors agree with the publication of this Corrigendum, and are grateful to the Editor of Oncology Letters for allowing them the opportunity to publish this Corrigendum; moreover, they apologize to the readership for any inconvenience caused.

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Copy and paste a formatted citation
Spandidos Publications style
Zhou N, Si Z, Li T, Chen G, Zhang Z and Qi H: [Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis. Oncol Lett 32: 477, 2026.
APA
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., & Qi, H. (2026). [Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis. Oncology Letters, 32, 477. https://doi.org/10.3892/ol.2026.15832
MLA
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., Qi, H."[Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis". Oncology Letters 32.4 (2026): 477.
Chicago
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., Qi, H."[Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis". Oncology Letters 32, no. 4 (2026): 477. https://doi.org/10.3892/ol.2026.15832
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou N, Si Z, Li T, Chen G, Zhang Z and Qi H: [Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis. Oncol Lett 32: 477, 2026.
APA
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., & Qi, H. (2026). [Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis. Oncology Letters, 32, 477. https://doi.org/10.3892/ol.2026.15832
MLA
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., Qi, H."[Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis". Oncology Letters 32.4 (2026): 477.
Chicago
Zhou, N., Si, Z., Li, T., Chen, G., Zhang, Z., Qi, H."[Corrigendum] Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis". Oncology Letters 32, no. 4 (2026): 477. https://doi.org/10.3892/ol.2026.15832
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