Journal of cellular biochemistry最新文献

Mammals exhibit two distinct types of adipose depots: white adipose tissue (WAT) and brown adipose tissue (BAT). While WAT primarily functions as a site for energy storage, BAT serves as a thermogenic tissue that utilizes energy and glucose consumption to regulate core body temperature. Under specific stimuli such as exercise, cold exposure, and drug treatment, white adipocytes possess a remarkable ability to undergo transdifferentiation into brown-like cells known as beige adipocytes. This transformation process, known as the “browning of WAT,” leads to the acquisition of new morphological and physiological characteristics by white adipocytes. We investigated the potential role of Irisin, a 12 kDa myokine that is secreted in mice and humans by skeletal muscle after physical activity, in inducing the browning process in mesenchymal stromal cells (MSCs). A subset of the MSCs possesses the remarkable capability to differentiate into different cell types such as adipocytes, osteocytes, and chondrocytes. Consequently, comprehending the effects of Irisin on MSC biology becomes a crucial factor in investigating antiobesity medications. In our study, the primary objective is to evaluate the impact of Irisin on various cell types engaged in distinct stages of the differentiation process, including stem cells, committed precursors, and preadipocytes. By analyzing the effects of Irisin on these specific cell populations, our aim is to gain a comprehensive understanding of its influence throughout the entire differentiation process, rather than solely concentrating on the final differentiated cells. This approach enables us to obtain insights into the broader effects of Irisin on the cellular dynamics and mechanisms involved in adipogenesis.

This article corrects the following:

The new role of riluzole in the treatment of pancreatic cancer through the apoptosis and autophagy pathways

Rulin Sun, Xujun He, Xiaoting Jiang, Houquan Tao

J Cell Biochem 2021; 122: 934–944.

doi:10.1002/jcb.29533

First Published online: November 11, 2019

In the original version of this article, the authors selected the wrong image to depict migration inhibition of PANC1 cells treated with 200µM of riluzole, resulting in panel duplication. The correct Figure 3B is shown below.

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

The above article, published online on 28 March 2019 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.28599) 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. 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.

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.

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.