Journal of cellular biochemistry最新文献

Downregulation of miR-218 by nicotine promotes cell proliferation through targeting CDK6 in non–small cell lung cancer, by Zhen Liu, Cuiling Lu, Guanren Zhao, Xue Han, Kaisheng Dong, Chuanhai Wang, Jing-Zhi Guan, Zhongyuan Wang, J Cell Biochem. 2019; 120: 18370-18377: The above article, published online on 12 June 2019 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.29148) has been retracted by agreement between the authors, the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. The authors were not able to provide comprehensive experimental data upon request. Accordingly, the conclusions of this article must be considered insufficiently supported.

Retraction: “Quercetin improve ischemia/reperfusion-induced cardiomyocyte apoptosis in vitro and in vivo study via SIRT1/PGC-1α signaling”, by Jiayou Tang, Linhe Lu, Yang Liu, Jipeng Ma, Lifang Yang, Lanlan Li, Hong Guo, Shiqiang Yu, Jun Ren, Heping Bai, Jian Yang, J Cell Biochem. 2019; 120: 9747-9757: The above article, published online on 17 January 2019 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.28255) has been retracted by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, image elements in Figure 4 were found to have been previously published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. The authors did not respond when asked to collaborate during the investigation and confirm the retraction.

Retraction: “MicroRNA-205 affects mouse granulosa cell apoptosis and estradiol synthesis by targeting CREB1,” by Pengju Zhang, Jun Wang, Hongyan Lang, Weixia Wang, Xiaohui Liu, Haiyan Liu, Chengcheng Tan, Xintao Li, Yumin Zhao, Xinghong Wu, J Cell Biochem. 2018; 120: 8466-8474: The above article, published online on 16 December 2018 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.28133) has been retracted by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The retraction has been agreed following an investigation based on allegations raised by third parties. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, multiple image duplications as well as image elements that were published previously in a different scientific context were found in Figures 2, 3, and 5. Thus, the editors consider the conclusions of this article to be invalid. The authors did not respond when asked to collaborate during the investigation and confirm the retraction.

Withdrawn: ‘LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis’ by Su Ni, Chao Xu, Chao Zhuang, Gongyin Zhao, Chenkai Li, Yuji Wang, Xihu Qin, J Cell Biochem (https://doi.org/10.1002/jcb.29637). The above article, published online on 7 February 2020 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcb.29637) has been withdrawn by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The withdrawal has been agreed following no response from the author to requests to sign the Journal's publishing license.

Retraction: “MiR-137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP” by Feng Ding, Shuang Zhang, Shaoyang Gao, Jian Shang, Yanxia Li, Ning Cui, and Qiu Zhao, J Cell Biochem. 2018; 4799-4807: The above article, published online on 13 January 2018 in Wiley Online Library (https://doi.org/10.1002/jcb.26676) has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC.

The retraction has been agreed after the authors stated that errors occurred during figure compilation, and that the experimental data in the article could not be verified. The investigation additionally revealed inconsistencies in several image elements. Thus, the editors consider the conclusions of this article to be invalid.

In the original version of this article, the authors wrongly assembled panels for the Western Blots presented in Figure 5. The loading controls chosen do not originate from the same blots depicting the expression levels of the proteins of interest. The correct Figure 5 is shown below.

This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.

Hao Sun, Shu Hu, Ziji Zhang, Jiayong Lun, Weiming Liao, Zhiqi Zhang

In the original version of this article, the authors wrongly assembled Figure 5A resulting in the IHC staining of SOX9 for the hBMSC-320c-Exos group to be mistakenly used in both Figures 5A and 5B. The correct Figure 5A is shown below.

This correction doesn't change the results and conclusions. The authors apologize for any confusion this error may have caused.

Over recent years, the investigation of transposable elements (TEs) has granted researchers a deeper comprehension of their characteristics and functions, particularly regarding their significance in the mechanisms contributing to cancer development. This manuscript focuses on prostate carcinoma cell lines and offers a comprehensive review intended to scrutinize the associations and interactions between TEs and genes, as well as their response to treatment using various chemical drugs, emphasizing their involvement in cancer progression. We assembled a compendium of articles retrieved from the PubMed database to construct networks demonstrating correlations with genes and pharmaceuticals. In doing so, we linked the transposition of certain TE types to the expression of specific transcripts directly implicated in carcinogenesis. Additionally, we underline that treatment employing different drugs revealed unique patterns of TE reactivation. Our hypothesis gathers the current understanding and guides research toward evidence-based investigations, emphasizing the association between antiviral drugs, chemotherapy, and the reduced expression of TEs in patients affected by prostate cancer.

Neuregulin-4 (Nrg4) and melatonin play vital roles in endocrine diseases. However, there is little discussion about the function and potential mechanism of Nrg4 and melatonin in prolactin (PRL) regulation. The human normal pituitary data from Gene Expression Profiling Interactive Analysis (GEPIA) database was used to explore the correlation between NRG4 and PRL. The expression and correlation of NRG4 and PRL were determined by Immunofluorescence staining (IF) and human normal pituitary tissue microarray. Western Blot (WB) was used to detect the expression of PRL, p-ErbB2/3/4, ErbB2/3/4, p-Erk1/2, Erk1/2, p-Akt and Akt in PRL-secreting pituitary GH3 and RC-4B/C cells treated by Nrg4, Nrg4-small interfering RNA, Erk1/2 inhibitor FR180204 and melatonin. The expression of NRG4 was significantly positively correlated with that of PRL in the GEPIA database and normal human pituitary tissues. Nrg4 significantly increased the expression and secretion of PRL and p-Erk1/2 expression in GH3 cells and RC-4B/C cells. Inhibition of Nrg4 significantly inhibited PRL expression. The increased levels of p-Erk1/2 and PRL induced by Nrg4 were abolished significantly in response to FR180204 in GH3 and RC-4B/C cells. Additionally, Melatonin promotes the expression of Nrg4, p-ErbB4, p-Erk1/2, and PRL and can further promote the expression of p-Erk1/2 and PRL in combination with Nrg4. Further investigation into the function of Nrg4 and melatonin on PRL expression and secretion may provide new clues to advance the clinical control of prolactinomas and hyperprolactinemia.

Mesenchymal stem cells (MSCs) display unique homing and immunosuppression features which make them promising candidates for cell therapy in inflammatory disorders. It is known that C-X-C chemokine receptor type 4 (CXCR4, also known as CD184) is a critical receptor implicated in MSCs migration, and the protein programmed death ligand-1 (PD-L1) is involved in MSC's immunosuppression. However, it remains unclear how the molecular mechanisms regulate PD-L1 expression for migration and immunosuppression of MSCs under the inflammatory microenvironment. In this article, we used the human adipose-derived mesenchymal stem cells (hADMSCs) treated with lipopolysaccharide (LPS) as an in vitro inflammatory model to explore the roles of PD-L1 on the migration and immunosuppression of MSC. Our results demonstrate that in hADMSCs, LPS significantly increased PD-L1 expression, which mediated the migration of the LPS-treated hADMSCs via CXCR4. In addition, we found that the increased PD-L1 expression in the LPS-treated hADMSCs inhibited B cell proliferation and immunoglobulin G secretion through nuclear factor-κB. Our study suggests that the PD-L1 plays critical roles in the homing and immunosuppression of MSCs which are a promising cell therapy to treat inflammatory diseases.