FEBS Open Bio最新文献

FEBS-IUBMB-ENABLE Conference crosses seven seas: Report on the 3rd International Molecular Biosciences PhD and Postdoc Conference—“Artificial intelligence: reshaping biomedical and healthcare research” FEBS-IUBMB-ENABLE会议跨越七大洋：第三届国际分子生物科学博士和博士后会议报告-“人工智能：重塑生物医学和医疗保健研究”

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-27 DOI: 10.1002/2211-5463.70031

Kaustuv Ghosh, Dayang Asyiqin

{"title":"FEBS-IUBMB-ENABLE Conference crosses seven seas: Report on the 3rd International Molecular Biosciences PhD and Postdoc Conference—“Artificial intelligence: reshaping biomedical and healthcare research”","authors":"Kaustuv Ghosh, Dayang Asyiqin","doi":"10.1002/2211-5463.70031","DOIUrl":"https://doi.org/10.1002/2211-5463.70031","url":null,"abstract":"The 3rd FEBS-IUBMB-ENABLE International Molecular Biosciences PhD and Postdoc Conference was held for the first time outside Europe, in South East Asia. On 4–6 December 2024, the Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, hosted over 260 participants from all around the world. The theme of this year's conference was “Artificial Intelligence – Reshaping biomedical and healthcare research”. The conference included a 2-day scientific symposium subdivided into four sessions: “AI in metabolic diseases, population and global health”, “AI in neuroscience and mental health”, “AI in respiratory and infectious diseases” and “AI in skin diseases and wound repair”. Ten global experts working at the forefront of expanding these horizons using AI were hosted. Through over 40 talks and 80 poster presentations, the participants at the conference, mostly young scientists at the doctoral and postdoctoral levels, had the chance to exhibit their research, fostering scientific exchange and collaboration. The last day of the conference included a career day dedicated to workshops, career sharing sessions and a panel discussion, where the focus was on career development, personal well-being, and translating academic research into industry innovations and startups. Pre-conference activities aimed towards fostering camaraderie and creating lasting memories made it a ‘must-to-attend’ event. The legacy of this conference will be carried forward by the next edition of FEBS-IUBMB-ENABLE titled “Bridging minds – Interdisciplinary research for the future of life sciences”, that will be hosted by Cancer Research UK (CRUK) Scotland Institute in Glasgow, UK, on 10–12 September 2025.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 S1","pages":"3-13"},"PeriodicalIF":2.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.70031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

GDP-fucose transporter SLC35C1: a potential regulatory role in cytosolic GDP-fucose and fucosylated glycan synthesis. GDP聚焦转运蛋白SLC35C1：在胞质GDP聚焦和聚焦聚糖合成中的潜在调节作用。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-27 DOI: 10.1002/2211-5463.70057

Edyta Skurska, Mariusz Olczak

{"title":"GDP-fucose transporter SLC35C1: a potential regulatory role in cytosolic GDP-fucose and fucosylated glycan synthesis.","authors":"Edyta Skurska, Mariusz Olczak","doi":"10.1002/2211-5463.70057","DOIUrl":"https://doi.org/10.1002/2211-5463.70057","url":null,"abstract":"Glycosylation occurs mainly in the Golgi apparatus, whereas the synthesis of nucleotide sugars occurs in the cytoplasm or nucleus. GDP-fucose in mammalian cells could be produced via de novo and salvage pathways in the cytoplasm; the first one is responsible for about 90% of GDP-fucose in the total pool of this nucleotide sugar in the cell. SLC35C1 (C1) is the primary transporter of GDP-fucose to the Golgi apparatus. In the absence of this transporter, it was proposed that nucleotide sugar could still reach the Golgi apparatus via a SLC35C2, the homologue of SLC35C1. However, simultaneous inactivation of the two transporters did not influence GDP-fucose transport across the Golgi apparatus membranes after external fucose supplementation. In this study, we combined the inactivation of SLC35C1 and enzymes of the GDP-fucose biosynthesis pathways (FCSK, GMDS and TSTA3) to study the impact of double inactivation on the production of nucleotide sugar and fucosylated glycans. We found that a lack of SLC35C1 changed the level of enzymes of both de novo and salvage pathways. Upon fucose supplementation, stimulation of the salvage pathway was remarkably high in the absence of the TSTA3 protein, and the concentration of GDP-fucose increased to millimolar values. In this work, we discovered that simultaneous deficiency of the SLC35C1 protein and TSTA3 enzyme increased GDP-fucose production via the salvage pathway to an even higher level. Finally, we found that nucleotide sugar still accessed the Golgi apparatus and had differential effects on N- and O-glycans.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Identifying prognostic targets in metastatic prostate cancer beyond AR. 识别转移性前列腺癌的预后靶点。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-22 DOI: 10.1002/2211-5463.70059

Emily Feng, Eric Feng, Tracy Berg, Isabella S Nguyen, Lilac G Nguyen, William Chen, Meng Zhang, David Quigley, Marina Sharifi, Haolong Li, Ilsa Coleman, Peter S Nelson, Martin Sjöström, Shuang G Zhao

{"title":"Identifying prognostic targets in metastatic prostate cancer beyond AR.","authors":"Emily Feng, Eric Feng, Tracy Berg, Isabella S Nguyen, Lilac G Nguyen, William Chen, Meng Zhang, David Quigley, Marina Sharifi, Haolong Li, Ilsa Coleman, Peter S Nelson, Martin Sjöström, Shuang G Zhao","doi":"10.1002/2211-5463.70059","DOIUrl":"https://doi.org/10.1002/2211-5463.70059","url":null,"abstract":"Genome-wide screens using CRISPR/RNAi can identify new therapeutic vulnerabilities in prostate cancer. In this study, we combine DepMap functional screen data with a large gene expression database (N = 1012) and clinical outcomes to identify potentially druggable targets. Eight genes (CYC, CYP51A1, DHFR, EBP, KIF15, PPM1D, SQLE, and UMPS) demonstrated strong dependency in cell lines and were also associated with worse prognosis clinically, representing potential therapeutic targets in metastatic prostate cancer. Four of these (DHFR, EBP, KIF15, and PPM1D) demonstrated higher expression in neuroendocrine prostate cancer. Furthermore, all but one (KIF15) were not significantly decreased from pretreatment to posttreatment, suggesting that they may remain targetable postabiraterone therapy. All eight genes showed evidence of protein expression in prostate cancers or cell lines. These potentially druggable targets associated with prostate cancer cell line dependency and worse clinical outcomes have also demonstrated literature support as potential targets, supporting further research into their potential clinical relevance as therapeutic targets in prostate cancer.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Short peptide perturbs spermatogenesis via immune microenvironment dysregulation and mitochondrial imbalance. 短肽通过免疫微环境失调和线粒体失衡干扰精子发生。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-22 DOI: 10.1002/2211-5463.70058

Heng Wang, Xiaofang Tan, Deyu Chen

{"title":"Short peptide perturbs spermatogenesis via immune microenvironment dysregulation and mitochondrial imbalance.","authors":"Heng Wang, Xiaofang Tan, Deyu Chen","doi":"10.1002/2211-5463.70058","DOIUrl":"https://doi.org/10.1002/2211-5463.70058","url":null,"abstract":"A short peptide derived from the occludin protein regulates tight junctions (TJ) of the blood-testis barrier and impairs germ cell development. However, the mechanism behind how this peptide regulates TJ and induces cell apoptosis remains unclear. In the present study, an animal model with induced TJ disruption via the short peptide was used to evaluate its impact on spermatogenesis. Here, we demonstrate that the short peptide promoted the infiltration of immune cells into the testicular interstitial tissue, accompanied by upregulation expression of the pro-inflammatory factors interleukin-6 and tumor necrosis factor-α. Moreover, mitochondrial fragmentation and mitophagy were upregulated in Sertoli cells and Leydig cells. Consistently, terminal deoxynucleotidyl transferase dUTP nick end labeling staining revealed extensive apoptosis in the testes during spermatogenesis. Notably, the severity of these disruptions began to attenuate after 27 days, although full functional recovery was not observed. Our findings reveal a novel mechanism wherein peptide-induced immune dysregulation and mitochondrial dysfunction synergistically impair spermatogenesis, potentially via microenvironmental perturbation of the TJ. Overall, these findings could hold valuable insights for the development of non-hormonal male contraceptives.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

FEM1B enhances TRAIL-induced apoptosis in T lymphocytes and monocytes. FEM1B增强trail诱导的T淋巴细胞和单核细胞凋亡。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-20 DOI: 10.1002/2211-5463.70056

Chenbo Yang, Wenhui Yu, Cui Dang, Jingjing Zhang, Jiahan Lu, Jing Xue

{"title":"FEM1B enhances TRAIL-induced apoptosis in T lymphocytes and monocytes.","authors":"Chenbo Yang, Wenhui Yu, Cui Dang, Jingjing Zhang, Jiahan Lu, Jing Xue","doi":"10.1002/2211-5463.70056","DOIUrl":"https://doi.org/10.1002/2211-5463.70056","url":null,"abstract":"FEM1B is recognized for its significant pro-apoptotic function in colorectal cancer; however, its influence and mechanisms regarding apoptosis in immune cells remain inadequately elucidated. In this study, we demonstrated that FEM1B enhances TRAIL-induced apoptosis in Molt-4, Jurkat, THP-1, and U937 cell lines. Notably, the knockdown of FEM1B in transfected cells resulted in a reversal of the observed increase in cell apoptosis. Our findings indicate that FEM1B activates caspase-3 and caspase-8, but not caspase-9, in response to TRAIL stimulation, suggesting its involvement in the extrinsic caspase-dependent apoptotic pathway. Furthermore, we found that FEM1B interacted with TRAF2 and downregulates its expression in Molt-4 and Jurkat cells, thereby diminishing TRAF2's inhibitory effect on caspase-8. In THP-1 and U937 cells, FEM1B was found to upregulate TRAIL-R2, thereby promoting TRAIL-induced apoptosis. Knockout studies in murine models further corroborated that FEM1B facilitates TRAIL-induced apoptosis. These results demonstrate that FEM1B enhances TRAIL-induced apoptosis in T lymphocytes and monocytes through a caspase-dependent mechanism involving TRAF2 or TRAIL receptors.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Boundaries of photosynthesis: adaptations of carbon fixation in extreme environments. 光合作用的边界：极端环境下的碳固定适应。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-19 DOI: 10.1002/2211-5463.70047

Pere Aguiló-Nicolau, Concepción Iñiguez, Sebastià Capó-Bauçà, Jeroni Galmés

引用次数: 0

Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss. 敲除线粒体拯救因子Ict1或Mtrfr在斑马鱼中是可行的，但在小鼠中不可行：每种因子损失背后的补偿机制。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-16 DOI: 10.1002/2211-5463.70054

Nobukazu Nameki, Chika Tomisawa, Soichiro Hoshino, Hidehiko Shimizu, Masashi Abe, Sho Arai, Kanako Kuwasako, Naoki Asakawa, Yusuke Inoue, Takuro Horii, Izuho Hatada, Masakatsu Watanabe

{"title":"Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss.","authors":"Nobukazu Nameki, Chika Tomisawa, Soichiro Hoshino, Hidehiko Shimizu, Masashi Abe, Sho Arai, Kanako Kuwasako, Naoki Asakawa, Yusuke Inoue, Takuro Horii, Izuho Hatada, Masakatsu Watanabe","doi":"10.1002/2211-5463.70054","DOIUrl":"https://doi.org/10.1002/2211-5463.70054","url":null,"abstract":"The mitochondrial translation system contains two ribosome rescue factors, ICT1 and MTRFR (C12orf65), which hydrolyze peptidyl-tRNA in stalled ribosomes. ICT1 also functions as a ribosomal protein of the mitochondrial large ribosomal subunit (mtLSU) in mice and humans, and its deletion is lethal. In contrast, MTRFR does not share this role. Although loss-of-function mutations in MTRFR have been linked to human mitochondrial diseases, data on this association in other vertebrates are lacking. Here, attempts to generate Mtrfr knockout mice were unsuccessful. However, knockout zebrafish lines were successfully generated for both ict1 and mtrfr (ict1-/- and mtrfr-/-). Both knockout lines appeared healthy and fertile. ict1-/-, mtrfr-/-, and wild-type adult caudal fin cells showed significant differences in mitochondrial morphology. The ict1 deletion affected the network properties more than the number of individuals and networks, whereas the mtrfr deletion exhibited the opposite effect. Additionally, the survival rates of the knockout line larvae were significantly lower than those of the wild-type larvae under starvation conditions. These results suggest that ict1 and mtrfr are required for survival under specific stress conditions, whereas ict1-/- and mtrfr-/- involve different compensatory mechanisms in response to loss of either factor under nonstress conditions. Ict1 proteins from all teleosts, including zebrafish, lack the N-terminal mtLSU-binding motif found in most metazoans, suggesting that Ict1 does not function as a ribosomal protein in teleosts. Thus, Mtrfr may partially compensate for the loss of Ict1. In conclusion, zebrafish appear to exemplify a limited category of vertebrates capable of enduring genetic abnormalities in ict1 or mtrfr.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Profiling the effect of low frequency mechanical vibration on the metabolic and oxidative stress responses of A431 carcinoma. 分析低频机械振动对A431癌代谢和氧化应激反应的影响。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-16 DOI: 10.1002/2211-5463.70055

Wresti L Anggayasti, Chikahiro Imashiro, Takashi Morikura, Shogo Miyata, Akira Funahashi, Kenjiro Takemura

{"title":"Profiling the effect of low frequency mechanical vibration on the metabolic and oxidative stress responses of A431 carcinoma.","authors":"Wresti L Anggayasti, Chikahiro Imashiro, Takashi Morikura, Shogo Miyata, Akira Funahashi, Kenjiro Takemura","doi":"10.1002/2211-5463.70055","DOIUrl":"https://doi.org/10.1002/2211-5463.70055","url":null,"abstract":"Mechanomedicine represents a potential biocompatible method in cancer therapy. In particular, the use of low-frequency mechanical vibration previously proved to trigger apoptosis of the human epidermoid carcinoma A431 cell line. In this study, we further characterized the metabolic and oxidative stress responses triggered by 1 h of 20 Hz mechanical vibration stimulus to A431 prior to cell death. Our results indicate that cell death may be related to the decrease of glucose consumption rate and the higher expression of reactive oxygen species right after mechanical stimulation (0 h). The overexpression of HMGB1 and HSP70 coding genes signified the increase of A431 cell stress. However, HMGB1 and HSP70 expression decreased at 24 h after mechanical vibration, along with the progression of cell death. We also observed cell morphology changes on A431 cells following vibration which might be indicative of A431 death by apoptosis. The emergence of these stress responses suggests that several pathways are connected to promote cancer cell death. The discovery of A431 cellular stress symptoms which lead to apoptotic death may clarify the usefulness of mechanical vibration in cancer treatment as a novel application of biomechanical manipulation.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Development of 4T1 breast cancer mouse model system for preclinical carbonic anhydrase IX studies. 用于临床前碳酸酐酶IX研究的4T1乳腺癌小鼠模型系统的建立。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-15 DOI: 10.1002/2211-5463.70052

Zane Kalniņa, Ilva Liekniņa, Svetlana Koteloviča, Ramona Petrovska, Gediminas Žvinys, Agne Petrosiute, Asta Zubrienė, Matīss Toms Laugalis, Vendija Skeltona, Juris Jansons, Madara Kreishmane, Edita Čapkauskaitė, Daumantas Matulis, Kaspars Tārs

{"title":"Development of 4T1 breast cancer mouse model system for preclinical carbonic anhydrase IX studies.","authors":"Zane Kalniņa, Ilva Liekniņa, Svetlana Koteloviča, Ramona Petrovska, Gediminas Žvinys, Agne Petrosiute, Asta Zubrienė, Matīss Toms Laugalis, Vendija Skeltona, Juris Jansons, Madara Kreishmane, Edita Čapkauskaitė, Daumantas Matulis, Kaspars Tārs","doi":"10.1002/2211-5463.70052","DOIUrl":"https://doi.org/10.1002/2211-5463.70052","url":null,"abstract":"Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer, for which targeted treatment is currently lacking. Carbonic anhydrase IX (CAIX) is a known cancer target due to its selective overexpression in hypoxia, a hallmark of many solid cancers including TNBC. This study aimed to develop a robust murine TNBC cell line 4T1-based model system that could be used in the comprehensive preclinical evaluation of targeting CAIX. The model is based on the original 4T1 breast cancer cell line and two genetically edited versions of it-one with biallelic CRISPR/Cas9-mediated Car9 inactivation and another with constitutively expressed Car9, thus ensuring negative and positive controls for CAIX production in the model system, respectively. The generated cell lines were validated for CAIX production and characterised functionally in vitro and in vivo after orthotopic implantation in syngeneic BALB/c mice. Results demonstrated significantly reduced primary tumour growth and metastatic progression rates in animals with CAIX-deficient tumours, while the CAIX-expressing tumours had vascularised phenotypes with prominent central areas of coagulative necrosis. The differential CAIX expression levels in the model were preserved during tumour growth in syngeneic mice, as verified by in vivo imaging using a novel high-affinity CAIX-specific near-infrared (NIR) fluorescent imaging probe, GZ22-4. Constitutive overexpression of autologous CAIX did not elicit specific autoantibody responses in vivo, demonstrating the suitability of this model for evaluating the efficacy of anti-CAIX vaccination as a therapeutic strategy. The in vivo study was repeated as an independent experiment and demonstrated good robustness of the developed model.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

RETRACTION: Fibronectin Enhances Tumor Metastasis Through B7-H3 in Clear Cell Renal Cell Carcinoma 结论：透明细胞肾细胞癌中纤维连接蛋白通过B7-H3促进肿瘤转移。

IF 2.8 4区生物学

FEBS Open Bio Pub Date : 2025-05-14 DOI: 10.1002/2211-5463.70053

{"title":"RETRACTION: Fibronectin Enhances Tumor Metastasis Through B7-H3 in Clear Cell Renal Cell Carcinoma","authors":"","doi":"10.1002/2211-5463.70053","DOIUrl":"10.1002/2211-5463.70053","url":null,"abstract":"RETRACTION: J. Xie, M. Sun, D. Zhang, C. Chen, S. Lin, and G. Zhang,“Fibronectin Enhances Tumor Metastasis Through B7-H3 in Clear Cell Renal Cell Carcinoma,” FEBS Open Bio 11, no. 11 (2021): 2977-2987, https://doi.org/10.1002/2211-5463.13280.The above article, published online on 25 August 2021 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Miguel De la Rosa; the Federation of European Biochemical Societies; and John Wiley & Sons Ltd. UK. The retraction has been agreed due to the discovery of duplications in Figures 2C and 5A. The authors originally reported these irregularities to the journal and offered corrected figures to replace the published figures. Upon the journal's analysis of the original image data, additional irregularities were found, including other image duplications with repositioning. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised. As a result, the Editor-in-Chief, FEBS Press, and John Wiley and Sons Ltd. have determined that a retraction is necessary. The authors agree with this decision.","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 6","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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