Cell Biochemistry and Function最新文献_第5页

Correction to “SIX1 Is Upregulated in Gastric Cancer and Regulates Proliferation and Invasion by Targeting the ERK Pathway and Promoting Epithelial-Mesenchymal Transition” 更正“SIX1在胃癌中上调并通过靶向ERK通路促进上皮-间质转化调控增殖和侵袭”

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2025-01-16 DOI: 10.1002/cbf.70045

{"title":"Correction to “SIX1 Is Upregulated in Gastric Cancer and Regulates Proliferation and Invasion by Targeting the ERK Pathway and Promoting Epithelial-Mesenchymal Transition”","authors":"","doi":"10.1002/cbf.70045","DOIUrl":"10.1002/cbf.70045","url":null,"abstract":"<p>Y. Xie, P. Jin, X. Sun, T. Jiao, Y. Zhang, Y. Li, and M. Sun, “SIX1 Is Upregulated in Gastric Cancer and Regulates Proliferation and Invasion by Targeting the ERK Pathway and Promoting Epithelial-Mesenchymal Transition,” <i>Cell Biochemistry and Function</i> 36, no. 8 (2018): 413–419, https://doi.org/10.1002/cbf.3361.</p><p>In the legend for Figure 2D of the published article, “HGC-7901” should be corrected to “HGC-27”. Additionally, reference 16 of the published article should be corrected to [1]:</p><p>H. Lv, A. Cui, F. Sun, Y. Zhang, Y. Li, L. Li, and Z. Lin, “Sineoculis Homeobox Homolog 1 Protein as an Independent Biomarker for Gastric Adenocarcinoma,” <i>Experimental and Molecular Pathology</i> 97, no. 1 (2014): 74–80, https://doi.org/10.1016/j.yexmp.2014.05.007.</p><p>The authors apologize for these errors and for the inconvenience these may have caused.</p><p><b>Reference</b></p><p>[1] H. Lv, A. Cui, F. Sun, Y. Zhang, Y. Li, L. Li, and Z. Lin, “Sineoculis Homeobox Homolog 1 Protein as an Independent Biomarker for Gastric Adenocarcinoma,” <i>Experimental and Molecular Pathology</i> 97, no. 1 (2014): 74–80, https://doi.org/10.1016/j.yexmp.2014.05.007.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000763","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}

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Progress in the Study of TAp73 and Sperm Apoptosis TAp73与精子凋亡的研究进展。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2025-01-11 DOI: 10.1002/cbf.70042

Ziao Liu, Min Pan, Jingya Li, Li Li, Tongsheng Wang

{"title":"Progress in the Study of TAp73 and Sperm Apoptosis","authors":"Ziao Liu, Min Pan, Jingya Li, Li Li, Tongsheng Wang","doi":"10.1002/cbf.70042","DOIUrl":"10.1002/cbf.70042","url":null,"abstract":"<div>\u0000 \u0000 <p>The study of the mechanism of oligoasthenospermia, which is a major cause of male infertility, has been the focus of research in the field of male reproduction. TAp73, a member of the p53 family of oncogenes, is endowed with tumor-suppressing activity due to its structural and functional homology with p53. It has been found that TAp73, plays a key role in spermatogenesis and maintaining male reproduction. When TAp73 is low-expressed or absent, the process of spermatogenesis is severely impaired, and mice deficient in TAp73 exhibit spermatogonial DNA damage, disturbed apical cytoplasmic specialization, and spermatocyte malformations resulting in reduced male fertility. Nevertheless, when TAp73 is overexpressed, it not only drives exogenous death receptors to regulate germ cell apoptosis, but also interacts with its various substrate proteins to promote the translocation of cytoplasmic Bax proteins to the mitochondria, resulting in the upregulation of the Bax/Bcl-2 ratio on the mitochondrial membrane and triggering a series of mitochondrial apoptotic effects. In this article, we will analyze the mechanism of TAp73 and sperm apoptosis, and elaborate the mechanism of TAp73 upregulation, exogenous apoptosis pathway and mitochondrial apoptosis pathway to systematically explain that the process of apoptosis induced by high expression of TAp73 is not fixed and single, but is interconnected, so as to provide a basis for the treatment of oligoasthenospermia and the research and development of new drugs using TAp73 as a target.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969699","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

Correction to “Gold Nanoparticles-Conjugated Quercetin Induces Apoptosis via Inhibition of EGFR/PI3K/Akt-Mediated Pathway in Breast Cancer Cell Lines (MCF-7 and MDA-MB-231)’’ 更正“金纳米颗粒结合槲皮素通过抑制乳腺癌细胞系（MCF-7和MDA-MB-231）中EGFR/PI3K/ akt介导的途径诱导细胞凋亡”。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2025-01-02 DOI: 10.1002/cbf.70041

引用次数: 0

Biocompatibility of Novel Marine Collagen on Periodontal Ligament Fibroblasts: A Pathway to Enhanced Regenerative Therapies 新型海洋胶原在牙周韧带成纤维细胞上的生物相容性：增强再生治疗的途径。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-31 DOI: 10.1002/cbf.70040

Yasir Dilshad Siddiqui, Erry Mochamad Arief, Muhammad Aliyan Saddique

引用次数: 0

Mettl14 and Mettl3 Work Cooperatively to Regulate Retinal Development Mettl14和Mettl3协同调节视网膜发育。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-31 DOI: 10.1002/cbf.70039

Dan Chen, Yanling Xin, Jingyi Guo, Shuyi Chen

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Vitamin D and Endometriosis: Is There a Mechanistic Link? 维生素D与子宫内膜异位症：是否存在机制联系？

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-31 DOI: 10.1002/cbf.70037

Bethany Scout Jennings, Martin Hewison

{"title":"Vitamin D and Endometriosis: Is There a Mechanistic Link?","authors":"Bethany Scout Jennings, Martin Hewison","doi":"10.1002/cbf.70037","DOIUrl":"10.1002/cbf.70037","url":null,"abstract":"<p>Endometriosis is a prevalent chronic gynaecological disorder, but its cause is still unclear, and both genetic and environmental factors may contribute disease aetiology. Prominent amongst the latter is vitamin D which can be obtained either by the action of sunlight on skin or from dietary sources. Serum levels of the main circulating form of vitamin D, 25-hydroxvitamin D (25(OH)D), have been reported to be inversely correlated with endometriosis, suggesting that vitamin D-deficiency may be a risk factor for the disease. Crucially, the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)<sub>2</sub>D) is known to exert many functions beyond its established role in the endocrinology of mineral homoeostasis and prevention of rickets. Several of these extra-skeletal effects of 1,25(OH)<sub>2</sub>D may impact the risk and progression of endometriosis. The following review details the studies that have assessed associations between vitamin D status/supplementation and endometriosis severity and disease progression, but also describes the mechanistic targets for 1,25(OH)<sub>2</sub>D in endometriosis with specific reference to immunomodulatory responses and effects on angiogenesis. Endometriosis is an under-reported health issue with poor non-invasive options for diagnosis. Given that vitamin D-deficiency may trigger or exacerbate key pathophysiological responses linked to endometriosis, analysis of vitamin D status in women may provide an alternative risk marker for endometriosis. Treatment options for endometriosis are also limited and the review will also consider whether vitamin D supplementation has a role in the management of endometriosis, either in prevention or treatment.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11686426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909488","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

Shh Protects the Injured Spinal Cord in Mice by Promoting the Proliferation and Inhibiting the Apoptosis of Nerve Cells via the Gli1–TGF–β1/ERK Axis Shh通过Gli1-TGF-β1/ERK轴促进神经细胞增殖和抑制细胞凋亡，从而保护小鼠损伤脊髓。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-29 DOI: 10.1002/cbf.70038

Yunfei Liu, Meihua Hou, Jingran Wang, Xiaoying Li, Bichao Zhang, Juntang Lin, Ciqing Yang

{"title":"Shh Protects the Injured Spinal Cord in Mice by Promoting the Proliferation and Inhibiting the Apoptosis of Nerve Cells via the Gli1–TGF–β1/ERK Axis","authors":"Yunfei Liu, Meihua Hou, Jingran Wang, Xiaoying Li, Bichao Zhang, Juntang Lin, Ciqing Yang","doi":"10.1002/cbf.70038","DOIUrl":"10.1002/cbf.70038","url":null,"abstract":"<div>\u0000 \u0000 <p>Spinal cord injury (SCI) is a common neurological trauma that cannot be completely cured with surgical techniques and medications. In this study, we established a mouse SCI model and used an adeno-associated virus (AAV) to achieve the high expression of sonic hedgehog (Shh) at the injury site to further investigate the therapeutic effect and mechanism of Shh on SCI. The results of the present study show that Shh may promote motor function recovery. The present findings demonstrate the protective effect of Shh overexpression in SCI by regulating the proliferation and apoptosis of nerve cells at the site of SCI. Shh promotes the proliferation of early microglia, inhibits the proliferation of early astrocytes, and promotes the formation of neurons at the site of injury. In addition, Shh may inhibit apoptosis at the SCI site. The mechanism by which Shh regulates nerve cells at the site of SCI may involve glioma-associated oncogene 1 (Gli1). The present research indicates that Gli1 regulates the transforming growth factor-β (TGF-β) signaling pathway, inhibiting the classic TGF-β1/Smad signaling pathway and activating the TGF-β1/extracellular regulated protein kinase (ERK) signaling pathway. Collectively, these findings suggest that Shh is a regulatory molecule involved in nerve cell proliferation and apoptosis. High Shh expression can accelerate motor function recovery after SCI, indicating that it may be a promising therapeutic approach for SCI.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920901","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

Identification of Potential Genes in Rheumatoid Arthritis-Associated Interstitial Lung Disease Using RNA-seq and In Vitro Analyses 利用RNA-seq和体外分析鉴定类风湿关节炎相关间质性肺疾病的潜在基因

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-26 DOI: 10.1002/cbf.70033

Liu-yan Nie, Kun Zhao, Cheng Xu, Wen-juan Zhang, Xin Huang, Yong-mei Han

{"title":"Identification of Potential Genes in Rheumatoid Arthritis-Associated Interstitial Lung Disease Using RNA-seq and In Vitro Analyses","authors":"Liu-yan Nie, Kun Zhao, Cheng Xu, Wen-juan Zhang, Xin Huang, Yong-mei Han","doi":"10.1002/cbf.70033","DOIUrl":"10.1002/cbf.70033","url":null,"abstract":"<div>\u0000 \u0000 <p>Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is an increasingly recognized extra-articular manifestations (EAMs) in the RA, with highly morbidity and mortality. The identification of key molecules involved in RA-ILD has a high requirement in clinic, and the role of their transcriptional regulation in the etiology of RA-ILD is great significant for investigation. In this study, we collected the whole peripheral blood samples of RA-ILD and RA only patients to bulk RNA-sequence. Differential gene expression analysis was employed to identify key genes, common pathways, and potential drug targets for RA-ILD. Furthermore, RT-qPCR was conducted to verify potential biomarkers in RA-ILD. Four hundred seventy-eight differentially expressed genes (DEGs) were identified that related to chromatin-modifying enzymes. A robust correlation with immune and inflammation biological processes and pathways was indicated through enrichment analyses of these shared DEGs, like B cell receptor signaling pathway, complement activation, NF-kappa B signaling pathway. Protein–protein interaction network analysis further emphasized the significance of 12 hub genes, including CHD4, MUS81, CXCL8, NSUN6, RAD9A, CCL4, B3GAT1, KAT2A, TBX21, HDAC2, ERBB2, and ITGAL. Notably, NSUN6 expression was statistically significant in RA-ILD by the machine learning LASSO regression analysis and RT-qPCR. Our study provides novel insights into the molecular mechanisms of RA-ILD, identifies potential biomarkers, and lays the groundwork for future therapeutic strategies.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892360","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 Between Autophagy and the Inflammasome in Human Tumors: Implications for the Treatment of Human Cancers 人类肿瘤中自噬与炎性体的相互作用：对人类癌症治疗的启示。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-25 DOI: 10.1002/cbf.70035

Qing Xia, Jingzhou Zhang

{"title":"Interaction Between Autophagy and the Inflammasome in Human Tumors: Implications for the Treatment of Human Cancers","authors":"Qing Xia, Jingzhou Zhang","doi":"10.1002/cbf.70035","DOIUrl":"10.1002/cbf.70035","url":null,"abstract":"<div>\u0000 \u0000 <p>Autophagy is a physiologically regulated cellular process orchestrated by autophagy-related genes (ATGs) that, depending on the tumor type and stage, can either promote or suppress tumor growth and progression. It can also modulate cancer stem cell maintenance and immune responses. Therefore, targeted manipulation of autophagy may inhibit tumor development by overcoming tumor-promoting mechanisms. The inflammasome is another multifunctional bioprocess that induces a form of pro-inflammatory programmed cell death, called pyroptosis. Dysregulation or overactivation of the inflammasome has been implicated in tumor pathogenesis and development. Additionally, autophagy can inhibit the NLRP3 inflammasome by removing inflammatory drivers. Recent research suggests that the NLRP3 inflammasome, in turn, affects autophagy. Understanding the complex interplay between autophagy and inflammasomes could lead to more precise and effective strategies for cancer treatments. In this review, we summarize the impact of autophagy and inflammasome dysregulation on tumor progression or suppression. We then highlight their targeting for cancer treatment as monotherapy or in combination with other therapies. Furthermore, we discuss the interaction between autophagy and tumor-promoting inflammation or the NLRP3 inflammasome. Finally, based on recent findings, we review the potential of this interaction for cancer treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892366","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

Epigenetic Regulation by Histone Methylation and Demethylation in Freeze-Tolerant Frog Kidney 耐冻蛙肾中组蛋白甲基化和去甲基化的表观遗传调控

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-12-20 DOI: 10.1002/cbf.70036

Olawale O. Taiwo, Sarah A. Breedon, Kenneth B. Storey

引用次数: 0