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      Correction: MicroRNA-302a Suppresses Tumor Cell Proliferation by Inhibiting AKT in Prostate Cancer

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      The PLOS ONE Editors
      PLoS ONE
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          Abstract

          After this article [1] was published, concerns were raised about overlap in content between this article and another article that was published in PLOS ONE by different authors and retracted in 2015 [2, 3]. There is substantial overlap in text, and multiple figures appear similar or identical across the two articles although labels and legends indicate that the data were obtained from different cell and tissue types (colon cancer cell lines and tissues in the retracted article [2] versus prostate cancer cell lines and tissues in [1]). The PLOS ONE Editors conducted follow up enquiries in response to the related article concerns. The authors of [1] provided PLOS ONE with raw image files and underlying data for this study, as well as approval documents issued by the Animal Studies Ethics Committee of Fudan University Medical School and the Ethics Committee of Fudan University Shanghai Cancer Center. In addition, the head of the Division of Scientific Research, Shanghai Cancer Center, Fudan University, confirmed the research and submission history reported by the authors for [1] based on the outcome of a prior investigation by Fudan University. Upon following up with the authors of the other article [2], the PLOS ONE Editors were unable to verify the integrity of that work, and as a result that article was retracted [3]. In light of the above information and documentation received from the authors of [1], the PLOS ONE Editors consider the related manuscript issue as resolved. The ethics approval documents provided in post-publication discussions indicated that the names of approving committees were incorrectly listed in the published Ethics Statement for this article [1]. The Ethics Statement is updated to: The use of patient samples was approved by the Ethics Committee of Fudan University Shanghai Cancer Center and signed informed consent was obtained from all study participants. The animal experiments were approved by the Animal Studies Ethics Committee of Fudan University Medical School. In addition, the published Data Availability Statement for this article is incorrect. The statement is updated to: All original underlying data for the study are available and will be provided upon request.

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          MicroRNA-302a Suppresses Tumor Cell Proliferation by Inhibiting AKT in Prostate Cancer

          Micro (mi) RNAs are important regulators involved in various physical and pathological processes, including cancer. The miRNA-302 family has been documented as playing a critical role in carcinogenesis. In this study, we investigated the role of miRNA-302a in prostate cancer (PCa). MiRNA-302a expression was detected in 44 PCa tissues and 10 normal prostate tissues, and their clinicopathological significance was analyzed. Cell proliferation and cell cycle analysis were performed on PCa cells that stably expressed miRNA-302a. The target gene of miRNA-302a and the downstream pathway were further investigated. Compared with normal prostate tissues, miRNA-302a expression was downregulated in PCa tissues, and was even lower in PCa tissues with a Gleason score ≥8. Overexpression of miRNA-302a induced G1/S cell cycle arrest in PCa cells, and suppressed PCa cell proliferation both in vitro and in vivo. Furthermore, miRNA-302a inhibits AKT expression by directly binding to its 3΄ untranslated region, resulting in subsequent alterations of the AKT-GSK3β-cyclin D1 and AKT-p27Kip1 pathway. These results reveal miRNA-302a as a tumor suppressor in PCa, suggesting that miRNA-302a may be used as a potential target for therapeutic intervention in PCa.
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            MicroRNA-302a Functions as a Putative Tumor Suppressor in Colon Cancer by Targeting Akt

            Micro RNAs (miRNAs) are important regulators involved in various physical and pathological processes, including cancer. The miRNA-302 family has been documented as playing a critical role in carcinogenesis. In this study, we investigated the role of miRNA-302a in colon cancer. MiRNA-302a expression was detected in 44 colon cancer tissues and 10 normal colon tissues, and their clinicopathological significance was analyzed. Cell proliferation and cell cycle analysis were performed on colon cancer cells that stably expressed miRNA-302a. The target gene of miRNA-302a and the downstream pathway were further investigated. Compared with normal colon tissues, miRNA-302a expression was downregulated in colon cancer tissues. Overexpression of miRNA-302a induced G1/S cell cycle arrest in colon cancer cells, and suppressed colon cancer cell proliferation both in vitro and in vivo. Furthermore, miRNA-302a inhibited AKT expression by directly binding to its 3′ untranslated region, resulting in subsequent alterations of the AKT-GSK3β-cyclin D1 pathway. These results reveal miRNA-302a as a tumor suppressor in colon cancer, suggesting that miRNA-302a may be used as a potential target for therapeutic intervention in colon cancer.
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              Retraction: MicroRNA-302a Functions as a Putative Tumor Suppressor in Colon Cancer by Targeting Akt

              (2015)
              It has been brought to the attention of the PLOS ONE editors that there is substantial overlap in content between this article and another article published in PLOS ONE by different authors: "MicroRNA-302a Suppresses Tumor Cell Proliferation by Inhibiting AKT in Prostate Cancer" (DOI: 10.1371/journal.pone.0124410) [2]. There is a substantial overlap in the text, and multiple figures appear similar or identical despite labels and legends indicating that the data were obtained from different cell and tissue types (prostate cancer cell lines and tissues in the above-mentioned article versus colon cancer cell lines and tissues in the retracted article). Our follow-up in relation to how the overlap with the article by Zhang et al. (DOI: 10.1371/journal.pone.0124410) [2] arose is ongoing. Upon our follow-up with the authors of the current article by Sun et al., we have been unable to obtain the underlying data and approval documents related to the study, and as a result, the PLOS ONE editors have been unable to verify the integrity of the work. In light of these concerns, the PLOS ONE editors retract this article.
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                Author and article information

                Journal
                PLoS One
                PLoS One
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                22 October 2020
                2020
                22 October 2020
                : 15
                : 10
                : e0241462
                Article
                PONE-D-20-32576
                10.1371/journal.pone.0241462
                7580994
                33091075
                6ac165f9-09fb-4fae-9556-721894a543f3
                © 2020 The PLOS ONE Editors

                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.

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