Journal of cellular biochemistry最新文献_第7页

RETRACTION: Downregulation of Fibroblast Growth Factor 5 Inhibits Cell Growth and Invasion of Human Nonsmall-Cell Lung Cancer Cells 回归：下调成纤维细胞生长因子 5 可抑制人类非小细胞肺癌细胞的生长和侵袭。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-11-08 DOI: 10.1002/jcb.30673

{"title":"RETRACTION: Downregulation of Fibroblast Growth Factor 5 Inhibits Cell Growth and Invasion of Human Nonsmall-Cell Lung Cancer Cells","authors":"","doi":"10.1002/jcb.30673","DOIUrl":"10.1002/jcb.30673","url":null,"abstract":"RETRACTION: Y. Zhou, Q. Yu, Y. Chu, X. Zhu, J. Deng, Q. Liu, Q. Wang, “Downregulation of Fibroblast Growth Factor 5 Inhibits Cell Growth and Invasion of Human Nonsmall-Cell Lung Cancer Cells,” Journal of Cellular Biochemistry 120, no. 5 (2019): 8238-8246. https://doi.org/10.1002/jcb.28107.The above article, published online on 05 December 2018, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The journal received notice from a third party regarding multiple images in this article which were published in other journals by different author groups, in which image was used in a different scientific context. The publisher confirmed that there is also duplication of images within Figure 3A of this article. The retraction has been agreed to because the evidence of image duplications both within this article and between different articles, each of which describes different experimental conditions, fundamentally compromises the conclusions presented in this article. The authors agree with the retraction.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 12","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30673","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shikonin Stimulates Mitochondria-Mediated Apoptosis by Enhancing Intracellular Reactive Oxygen Species Production and DNA Damage in Oral Cancer Cells 志贺宁通过增强口腔癌细胞的细胞内活性氧生成和 DNA 损伤来刺激线粒体介导的细胞凋亡

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-11-01 DOI: 10.1002/jcb.30671

Stuti Biswal, Munmun Panda, Bijesh Kumar Biswal

{"title":"Shikonin Stimulates Mitochondria-Mediated Apoptosis by Enhancing Intracellular Reactive Oxygen Species Production and DNA Damage in Oral Cancer Cells","authors":"Stuti Biswal, Munmun Panda, Bijesh Kumar Biswal","doi":"10.1002/jcb.30671","DOIUrl":"10.1002/jcb.30671","url":null,"abstract":"<div>\u0000 \u0000 Phytotherapy has rendered a new insight towards the treatment of various cancers, including oral cancer with fewer side effects, over the traditional chemotherapeutic drugs to overcome chemoresistance. Shikonin (Shk) is a natural biologically active alkaloid found in the Lithospermum erythrorhizon plant's root. It has potent cytotoxic activities against various cancers. Our study revealed the release time and anticancer potential of Shk on the SCC9 and H357 oral cancer cell lines. We investigated the antiproliferative, antimigratory, cell cycle arresting and apoptosis promoting activity of Shk in oral cancer cells by performing MTT and morphological assay, colony, and tumor sphere formation assay, AO/EtBr and DAPI staining, Annexin V-FITC/PI staining, assay for reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) measurement, comet assay, qRT-PCR, and western blot analysis. We also checked the interaction of DNA and Shk by docking and CD spectroscopy and EtBr displacement assay. As a result, we found that Shk reduced the viability, proliferation, and tumorigenicity of SCC9 and H357 cells in a time and concentration-dependent manner. We obtained half-maximal inhibitory concentration (IC50) at 0.5 µM for SCC9 and 1.25 µM for H357. It promotes apoptosis via overexpressing proapoptotic Bax and caspase 3 via enhancing ROS that leads to MMP depletion and DNA damage and arrests cells at the G2/M & G2/S phase. The antimigratory activity of Shk was performed by analyzing the expression of markers of epithelial–mesenchymal transition like E-cadherin, ZO-1, N-cadherin, and vimentin. These overall results recommended that Shk shows potent anticancer activity against oral cancer cell lines in both in vitro and ex vivo conditions. So, it could be an excellent agent for the treatment of oral cancer.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Effects and Mechanisms of Chrysosplenetin in Targeting RANKL-Induced NF-κB Signaling and NFATc1 Activation to Protect Bone Density in Osteolytic Diseases 金丝桃素靶向 RANKL 诱导的 NF-κB 信号和 NFATc1 激活以保护骨溶解性疾病患者骨密度的作用和机制

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-11-01 DOI: 10.1002/jcb.30670

Guoju Hong, Lin Zhou, Wei He, Qiushi Wei, Jiake Xu

{"title":"The Effects and Mechanisms of Chrysosplenetin in Targeting RANKL-Induced NF-κB Signaling and NFATc1 Activation to Protect Bone Density in Osteolytic Diseases","authors":"Guoju Hong, Lin Zhou, Wei He, Qiushi Wei, Jiake Xu","doi":"10.1002/jcb.30670","DOIUrl":"10.1002/jcb.30670","url":null,"abstract":"<div>\u0000 \u0000 Chrysosplenetin (CHR), an O-methylated flavonol from Chamomilla recutita and Laggera pterodonta, has previously demonstrated efficacy in enhancing osteoblast differentiation for treating postmenopausal osteoporosis. This study aims to evaluate CHR's potential to inhibit osteoclastogenesis and prevent bone deterioration in both in vitro and in vivo models. Using tartaric acid-resistant acid phosphatase staining and hydroxyapatite resorption assays, we examined the impact of CHR on RANKL-induced osteoclasts derived from mouse bone marrow monocytes. Additionally, Western blot analysis and qRT-PCR were utilized to assess the protein and gene expressions within the MAPK and NF-κB signaling pathways, as well as the NFATc1 pathway. In vivo, CHR's effects were validated using micro-CT and histomorphometry in an ovariectomized mouse model, showing significant reduction in osteoclast activity and bone loss. The study confirms CHR's inhibition of osteoclastogenesis through interference with RANKL-mediated signaling pathways, suggesting its potential as a novel therapeutic agent for osteolytic conditions related to osteoclast-osteoblast dysregulation.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Navigating the Roadblocks: Progress and Challenges in Cell-Based Therapies for Human Immunodeficiency Virus 路障导航：人类免疫缺陷病毒细胞疗法的进展与挑战》。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-11-01 DOI: 10.1002/jcb.30669

Lakshay Chhabra, Rajeev Kumar Pandey, Rajiv Kumar, Shyam Sundar, Sanjana Mehrotra

{"title":"Navigating the Roadblocks: Progress and Challenges in Cell-Based Therapies for Human Immunodeficiency Virus","authors":"Lakshay Chhabra, Rajeev Kumar Pandey, Rajiv Kumar, Shyam Sundar, Sanjana Mehrotra","doi":"10.1002/jcb.30669","DOIUrl":"10.1002/jcb.30669","url":null,"abstract":"<div>\u0000 \u0000 Cell-based therapies represent a major advancement in the treatment and management of HIV/AIDS, with a goal to overcome the limitations of traditional antiretroviral therapy (ART). These innovative approaches not only promise a functional cure by reconstructing the immune landscape but also address the persistent viral reservoirs. For example, stem cell therapies have emerged from the foundational success of allogeneic hematopoietic stem cell transplantation in curing HIV infection in a limited number of cases. B cell therapies make use of genetically modified B cells constitutively expressing broadly neutralizing antibodies (bNAbs) against target viral particles and infected cells. Adoptive cell transfer (ACT), including TCR-T therapy, CAR-T cells, NK-CAR cells, and DC-based therapy, is adapted from cancer immunotherapy and repurposed for HIV eradication. In this review, we summarize the mechanisms through which these engineered cells recognize and destroy HIV-infected cells, the modification strategies, and their role in sustaining remission in the absence of ART. The review also addresses the challenges to cell-based therapies against HIV and discusses the recent advancements aimed at overcoming them.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interaction of PGC7 and HP1BP3 Maintains Meg3-DMR Methylation by Regulating Chromatin Configuration PGC7和HP1BP3的相互作用通过调节染色质构型维持Meg3-DMR甲基化

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-18 DOI: 10.1002/jcb.30667

Yingxiang Liu, Weijie Hao, Chenyang Huang, Peiwen Feng, Hongliang Liu, Zekun Guo

{"title":"Interaction of PGC7 and HP1BP3 Maintains Meg3-DMR Methylation by Regulating Chromatin Configuration","authors":"Yingxiang Liu, Weijie Hao, Chenyang Huang, Peiwen Feng, Hongliang Liu, Zekun Guo","doi":"10.1002/jcb.30667","DOIUrl":"10.1002/jcb.30667","url":null,"abstract":"<div>\u0000 \u0000 Genomic imprinting is essential for mammalian development. PGC7, an important maternal factor, binds to dimethylated histone H3K9 (H3K9me2), maintaining DNA methylation in zygotes and stem cells. However, the underlying molecular mechanisms of PGC7-maintained genomic imprinting in stem cells are not clear. Our previous study has identified that PGC7 interacts with HP1BP3, a novel member of the histone H1 family. In this study, we found that PGC7 interacts with the central globular domain of HP1BP3 through its C-terminal tail and that HP1BP3 is responsible for the recruitment of PGC7 at the Meg3 differentially methylated region (DMR) in the Dlk1–Dio3 imprinted domain. HP1BP3 or PGC7 depletion decreases enrichment in the Meg3-DMR, leading to DNA hypermethylation in this region. Moreover, the cooperative binding of PGC7 and HP1BP3 can antagonize the enrichment of DNMT3A in the Meg3-DMR, and the depletion of HP1BP3 or PGC7 separately induces chromosome decondensation in this region. In summary, this is the first study demonstrating that PGC7 and HP1BP3 synergistically maintain the methylation status of the Meg3-DMR by enabling a chromatin configuration that interferes with the binding of the de novo DNA methyltransferase DNMT3A.</div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of Sodium-Dependent Vitamin C Transporter-2 and Ascorbate in Regulating the Hypoxic Pathway in Cultured Glioblastoma Cells 钠依赖性维生素 C 转运体-2 和抗坏血酸在调节培养胶质母细胞瘤细胞缺氧途径中的作用

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-09 DOI: 10.1002/jcb.30658

Eleanor R. Burgess, Citra Praditi, Elisabeth Phillips, Margreet C. M. Vissers, Bridget A. Robinson, Gabi U. Dachs, George A. R. Wiggins

{"title":"Role of Sodium-Dependent Vitamin C Transporter-2 and Ascorbate in Regulating the Hypoxic Pathway in Cultured Glioblastoma Cells","authors":"Eleanor R. Burgess, Citra Praditi, Elisabeth Phillips, Margreet C. M. Vissers, Bridget A. Robinson, Gabi U. Dachs, George A. R. Wiggins","doi":"10.1002/jcb.30658","DOIUrl":"10.1002/jcb.30658","url":null,"abstract":"The most common and aggressive brain cancer, glioblastoma, is characterized by hypoxia and poor survival. The pro-tumour transcription factor, hypoxia-inducible factor (HIF), is regulated via HIF-hydroxylases that require ascorbate as cofactor. Decreased HIF-hydroxylase activity triggers the hypoxic pathway driving cancer progression. Tissue ascorbate accumulates via the sodium-dependent vitamin C transporter-2 (SVCT2). We hypothesize that glioblastoma cells rely on SVCT2 for ascorbate accumulation, and that knockout of this transporter would disrupt the regulation of the hypoxic pathway by ascorbate. Ascorbate uptake was measured in glioblastoma cell lines (U87MG, U251MG, T98G) by high-performance liquid chromatography. CRISPR/Cas9 was used to knockout SVCT2. Cells were treated with cobalt chloride, desferrioxamine or 5% oxygen, with/without ascorbate, and key hypoxic pathway proteins were measured using Western blot analysis. Ascorbate uptake was cell line dependent, ranging from 1.7 to 11.0 nmol/106 cells. SVCT2-knockout cells accumulated 90%–95% less intracellular ascorbate than parental cells. The hypoxic pathway was induced by all three stimuli, and ascorbate reduced this induction. In the SVCT2-knockout cells, ascorbate had limited effect on the hypoxic pathway. This study verifies that intracellular ascorbate is required to suppress the hypoxic pathway. As patient survival is related to an activated hypoxic pathway, increasing intra-tumoral ascorbate may be of clinical interest.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Fibroblast Growth Factor-2 Promotes Catabolism via FGFR1-Ras-Raf-MEK1/2-ERK1/2 Axis That Coordinates With the PKCδ Pathway in Human Articular Chondrocytes 回归：成纤维细胞生长因子-2 通过 FGFR1-Ras-Raf-MEK1/2-ERK1/2 轴促进分解代谢，该轴与人关节软骨细胞中的 PKCδ 通路相协调。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-08 DOI: 10.1002/jcb.30665

{"title":"RETRACTION: Fibroblast Growth Factor-2 Promotes Catabolism via FGFR1-Ras-Raf-MEK1/2-ERK1/2 Axis That Coordinates With the PKCδ Pathway in Human Articular Chondrocytes","authors":"","doi":"10.1002/jcb.30665","DOIUrl":"10.1002/jcb.30665","url":null,"abstract":"RETRACTION: D. Yan, D. Chen, and H.-J. Im, “Fibroblast Growth Factor-2 Promotes Catabolism via FGFR1-Ras-Raf-MEK1/2-ERK1/2 Axis That Coordinates With the PKCδ Pathway in Human Articular Chondrocytes,” Journal of Cellular Biochemistry 113, no. 9 (2012): 2856-2865, https://doi.org/10.1002/jcb.24160.The above article, published online on 5 April 2012 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figures 2, 4 A and 5 C were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 12","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Propofol-Induced miR-219-5p Inhibits Growth and Invasion of Hepatocellular Carcinoma Through Suppression of GPC3-Mediated Wnt/β-Catenin Signalling Activation 回放：丙泊酚诱导的 miR-219-5p 通过抑制 GPC3 介导的 Wnt/β-Catenin 信号激活抑制肝细胞癌的生长和侵袭。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-08 DOI: 10.1002/jcb.30652

{"title":"RETRACTION: Propofol-Induced miR-219-5p Inhibits Growth and Invasion of Hepatocellular Carcinoma Through Suppression of GPC3-Mediated Wnt/β-Catenin Signalling Activation","authors":"","doi":"10.1002/jcb.30652","DOIUrl":"10.1002/jcb.30652","url":null,"abstract":"RETRACTION: T. Gong, X. Ning, Z. Deng, M. Liu, B. Zhou, X. Chen, S. Huang, Y. Xu, Z. Chen, and R. Luo, “Propofol-Induced miR-219-5p Inhibits Growth and Invasion of Hepatocellular Carcinoma Through Suppression of GPC3-Mediated Wnt/β-Catenin Signalling Activation,” Journal of Cellular Biochemistry 120, no. 10 (2019): 16934-16945, https://doi.org/10.1002/jcb.28952.The above article, published online on 19 May 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, multiple areas of overlap were detected within and across Figures 1D, 2E and 2F. The authors acknowledged that unintentional mistakes were made during figure compilation and collaborated on the investigation into the detected issues. Even though they provided the raw data underlying the study, verification of the material's accuracy proved challenging due to the time elapsed since publication. As full accuracy of the provided material could no longer be ascertained, the editors have decided to retract the article, as they consider the identified issues to undermine the reliability of the presented research. The authors agree with the decision of retraction acknowledging that the identified issues may impact the overall interpretation of the research findings.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30652","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: MiR-625-5p/PKM2 Negatively Regulates Melanoma Glycolysis State 返回：MiR-625-5p/PKM2 负向调节黑色素瘤的糖酵解状态。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-07 DOI: 10.1002/jcb.30651

{"title":"RETRACTION: MiR-625-5p/PKM2 Negatively Regulates Melanoma Glycolysis State","authors":"","doi":"10.1002/jcb.30651","DOIUrl":"10.1002/jcb.30651","url":null,"abstract":"RETRACTION: H. Zhang, C. Feng, M. Zhang, A. Zeng, L. Si, N. Yu, and M. Bai, “MiR-625-5p/PKM2 Negatively Regulates Melanoma Glycolysis State,” Journal of Cellular Biochemistry 120, no. 3 (2019): 2964–2972, https://doi.org/10.1002/jcb.26917.The above article, published online on 30 November 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The authors requested a retraction of this manuscript stating that different cell lines were wrongly labelled and that the conclusions of this manuscript needed to be re-evaluated. Further investigation by the publisher revealed that the article mentions use of the non-verifiable/unknown normal skin cells HFE. Additional flaws and inconsistencies between results presented and experimental methods described were identified. Furthermore, the experimental methods were found to lack sufficient details or have unavailable supporting data, making the experiments not comprehensible nor reproducible to readers. Accordingly, the editors consider the conclusions of this article to be invalid.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30651","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EXPRESSION OF CONCERN: Nrf2 Dependent Antiaging Effect of Milk-Derived Bioactive Peptide in Old Fibroblasts 表达关切：牛奶衍生生物活性肽对老年成纤维细胞的 Nrf2 依赖性抗衰老效应

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2024-10-07 DOI: 10.1002/jcb.30666

引用次数: 0