Advanced biology最新文献_第4页

Bacterial Quorum Sensing: A Double-Edged Sword in Cancer Development 细菌群体感应：癌症发展的双刃剑。

IF 2.6 3区生物学

Advanced biology Pub Date : 2025-07-21 DOI: 10.1002/adbi.202500023

Mirsadeghi Isfahani Paniz, Rastegar Lari Tina, Darbeheshti Farzaneh, Bahreini Farbod, Rezaei Nima

{"title":"Bacterial Quorum Sensing: A Double-Edged Sword in Cancer Development","authors":"Mirsadeghi Isfahani Paniz, Rastegar Lari Tina, Darbeheshti Farzaneh, Bahreini Farbod, Rezaei Nima","doi":"10.1002/adbi.202500023","DOIUrl":"10.1002/adbi.202500023","url":null,"abstract":"Cancer is one of the most pervasive and severe global diseases that cause millions of death annually. Numerous bacterial strains are found to play fundamental roles in tumor formation, growth, and metastasis. On the other hand, specific bacterial strains are discovered to induce beneficial changes to restrict tumoral growth and progression or alter the tumor microenvironment. Studies have also suggested bacteria are potential microorganisms that transfer synthetic genes or anti-tumor drugs. A particularly interesting area of study is bacterial communication, known as quorum sensing (QS), in which signal peptides adjust bacterial pathogenic traits such as virulence factor, drug resistance, and biofilm after a threshold volume of signals is reached. QS signals raised a propitious future perspective against diseases and cancer. Future comprehension of the QS system can lead to novel bacterial-based therapeutic procedures with the minimum healthy cell toxicity and higher target specificity rather than long-established methods. This review aims to highlight significant research and advancements in the field of QS to combat cancer and find more non-toxic and less-invasive treatments.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"9 9","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673700","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

LIN28B Promotes Cancer Cell Dissemination and Angiogenesis. LIN28B促进癌细胞扩散和血管生成。

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-07-18 DOI: 10.1002/adbi.202400730

Diana Corallo, Sara Menegazzo, Marcella Pantile, Silvia Bresolin, Carlo Zanon, Alessandro Davini, Massimiliano Mazzone, Alessandra Biffi, Sanja Aveic

{"title":"LIN28B Promotes Cancer Cell Dissemination and Angiogenesis.","authors":"Diana Corallo, Sara Menegazzo, Marcella Pantile, Silvia Bresolin, Carlo Zanon, Alessandro Davini, Massimiliano Mazzone, Alessandra Biffi, Sanja Aveic","doi":"10.1002/adbi.202400730","DOIUrl":"https://doi.org/10.1002/adbi.202400730","url":null,"abstract":"Neuroblastoma represents a major challenge in pediatric oncology with over 50% of cases involving metastasis. High-risk patients face an unfavorable prognosis, with survival rates below 40%. LIN28B plays a pivotal role in neuroblastoma development, being overexpressed in a subset of high-risk patients with widespread metastases. Here, the effect of induced LIN28B (iLIN28B) expression on neuroblastoma cells is investigated with a focus on key aspects of the metastatic cascade including anchorage, migration, invasion, and angiogenesis. iLIN28B cells show substrate-selective adherence, coating-dependent migration, and the context-guided ability to degrade the extracellular matrix. In response to tumor cell-derived IGF2, endothelial cells show enhanced motility and proliferation, while inhibition of IGF2 activity impairs LIN28B-induced angiogenesis in vitro and in vivo. These findings underscore the hub role of LIN28B in favoring pre-metastatic processes in neuroblastoma. The intricate interplay between LIN28B, endothelial cells, and the extracellular matrix contributes to the development of the aggressive neuroblastoma phenotypes.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00730"},"PeriodicalIF":3.2,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658077","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

Luteolin Regulates Mitophagy to Alleviate Myocardial Ischemia-Reperfusion Injury via Sirt3/Foxo3a Pathway. 木犀草素通过Sirt3/Foxo3a通路调节线粒体自噬减轻心肌缺血再灌注损伤

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-07-18 DOI: 10.1002/adbi.202400778

Li Yan, Lei Liang, Qiling Gou, Haoyu Wu, Mengya Dong, Hao Chen, Jiayu Diao

{"title":"Luteolin Regulates Mitophagy to Alleviate Myocardial Ischemia-Reperfusion Injury via Sirt3/Foxo3a Pathway.","authors":"Li Yan, Lei Liang, Qiling Gou, Haoyu Wu, Mengya Dong, Hao Chen, Jiayu Diao","doi":"10.1002/adbi.202400778","DOIUrl":"https://doi.org/10.1002/adbi.202400778","url":null,"abstract":"Luteolin (LUT) belongs to a kind of flavonoid, which has protective effects on myocardial ischemia/reperfusion (I/R) injury. Sirt3 is located in mitochondria and interacts with Foxo3a to protect mitochondrial function against stress. Mitophagy is an important form of mitochondrial quality control. However, whether LUT regulates mitophagy to alleviate myocardial I/R injury via the Sirt3/Foxo3a pathway is rarely reported. In this study, 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP) is used to inhibit the Sirt3/Foxo3a pathway. Male adult rats are divided into four groups: Sham group, I/R group, I/R+LUT group, and I/R+LUT+3-TYP group. The I/R rats model is established by ligating the left anterior descending coronary artery for 30 min, then releasing the ligature for 24 h. Indexes of left ventricular function, myocardial damage, oxidative stress, and mitophagy are detected. It is found that LUT treatment activated Sirt3/Foxo3a pathway, improves left ventricular function, decreases myocardial infarction size, inhibits myocardial apoptosis and oxidative stress, and initiates mitophagy in I/R rats. Moreover, these protective effects of LUT are weakened when Sirt3 is inhibited. Together, LUT regulates mitophagy to alleviate myocardial I/R injury via the Sirt3/Foxo3a pathway.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00778"},"PeriodicalIF":3.2,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658078","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

Label-Free Detection of Lipid Accumulation in Cells Using Magnetic Levitation (Adv. Biology 7/2025) 利用磁悬浮无标记检测细胞内脂质积累（ad . Biology 7/2025）

IF 2.6 3区生物学

Advanced biology Pub Date : 2025-07-15 DOI: 10.1002/adbi.70026

Kazim Kerim Moncal, Laeya Abdoli Najmi, Rakhi Gupta, Malavika Ramarao, Joshua W. Knowles, Chong Y. Park, Naside Gozde Durmus

引用次数: 0

Application of Immune Repertoire Analysis in Differentiating Thyroid Cancer and Large Benign Thyroid Nodules (Adv. Biology 7/2025) 免疫库分析在甲状腺癌与甲状腺大良性结节鉴别中的应用（ad . Biology 7/2025）

IF 2.6 3区生物学

Advanced biology Pub Date : 2025-07-15 DOI: 10.1002/adbi.70027

Jun Zhu, Xu Zhang, Xiangqing Zhu, Ziran Gao, Zhong Ni, Tiancheng Zhang, Meijin Huang

引用次数: 0

Inhibition of Glutamine Metabolism Attenuates Tumor Progression Through Remodeling of the Macrophage Immune Microenvironment. 抑制谷氨酰胺代谢通过重塑巨噬细胞免疫微环境减缓肿瘤进展。

IF 2.6 3区生物学

Advanced biology Pub Date : 2025-07-13 DOI: 10.1002/adbi.202400738

Tianhe Li, Sepehr Akhtarkhavari, Sumeng Qi, Jiawei Fan, Tu-Yung Chang, Yao-An Shen, JinMing Yang, Barbara S Slusher, Ie-Ming Shih, Stephanie Gaillard, Tian-Li Wang

{"title":"Inhibition of Glutamine Metabolism Attenuates Tumor Progression Through Remodeling of the Macrophage Immune Microenvironment.","authors":"Tianhe Li, Sepehr Akhtarkhavari, Sumeng Qi, Jiawei Fan, Tu-Yung Chang, Yao-An Shen, JinMing Yang, Barbara S Slusher, Ie-Ming Shih, Stephanie Gaillard, Tian-Li Wang","doi":"10.1002/adbi.202400738","DOIUrl":"10.1002/adbi.202400738","url":null,"abstract":"Targeting glutamine metabolism has emerged as a promising strategy in cancer therapy. To attain clinical utility, a number of challenges must be overcome, including in vivo anti-tumor activity, pharmacological toxicity, and clinical safety. Aside from glutamine-addicted tumor cells, immune cells may also need glutamine to sustain physiological activities; thus, the current work used two immunological-intact murine cancer models to assess the effects of glutamine antagonists on tumor cells and the immune milieu. To minimize potential off-target effects, we developed a glutamine antagonist prodrug, JHU083, which is bioactivated selectively in cancer tissues. In both murine tumor models, we observed a significant anti-tumor effect, resulting in reduced tumor burden and impeded tumor progression. Single-cell RNA sequencing of tumor tissues demonstrated that JHU083 significantly hampered the immunosuppressive M2-like macrophages but not the pro-inflammatory M1-like macrophages. Expression of Myc- and hypoxia-regulated genes were also inhibited by JHU083. Ex vivo bone marrow-derived macrophage cultures further confirmed that M2 macrophages were more sensitive to glutamine antagonist than M1 macrophages. Together, our findings indicate that JHU083 exerted its anti-tumor activity not only through direct targeting of glutamine-addicted cancer cells but also by shifting the M1/M2 macrophage landscape in favor of an immune-stimulatory microenvironment.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00738"},"PeriodicalIF":2.6,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625266","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

A Pan-Enterovirus Natural Product Inhibitor Targeting a Unique Allosteric Site on the Viral 3C Protease. 一种针对病毒3C蛋白酶独特变构位点的泛肠病毒天然产物抑制剂

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-07-10 DOI: 10.1002/adbi.202400845

Shangwu Sun, Qiang Wang, Mengyao Zhu, Xuan Zhang, Xianfang Zhang, Bei Yang

{"title":"A Pan-Enterovirus Natural Product Inhibitor Targeting a Unique Allosteric Site on the Viral 3C Protease.","authors":"Shangwu Sun, Qiang Wang, Mengyao Zhu, Xuan Zhang, Xianfang Zhang, Bei Yang","doi":"10.1002/adbi.202400845","DOIUrl":"https://doi.org/10.1002/adbi.202400845","url":null,"abstract":"Infections caused by Enterovirus like rhinoviruses, coxsackieviruses, and polioviruses represent a significant public health concern, for which there are no antivirals available yet. The highly conserved viral 3C protease has been the primary target for antiviral development, but competitive inhibitors targeting its active site does not meet expectations in clinical studies. Previously, an unconventional allosteric site is identified on human rhinovirus 14 (HRV14) 3C, representing novel opportunities for pan-enterovirus antivirals development. Here, in silico screening of 143,621 natural products against this allosteric site is performed and 28 candidate molecules are identified, among which dihydromyricetin (DHM) and oridonin-A1 bind to HRV14 3C and allosterically inhibit its protease activity. Moreover, DHM shows minimal cytotoxicity and potent antiviral efficacy against HRV14 infections across different cell models, with selective indexes exceeding 700. Structural analysis and mutagenesis assays further pinpoint key 3C residues essential for DHM binding. Consistent with the high conservation of these residues across Enterovirus genus, DHM broadly binds and efficiently inhibits 3C proteases from not only rhinoviruses, but also coxsackieviruses, enteroviruses and polioviruses. These findings establish DHM as a unique, broad-spectrum allosteric inhibitor of Enterovirus 3C proteases and underscore its potential as a promising candidate for the development of pan-enterovirus antivirals.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00845"},"PeriodicalIF":3.2,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599091","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

Research Progress on the Combination of PARP Inhibitors (PARPi) and Immune Checkpoint Inhibitors (ICIs) PARP抑制剂（PARPi）与免疫检查点抑制剂（ICIs）联合应用的研究进展。

IF 2.6 3区生物学

Advanced biology Pub Date : 2025-07-09 DOI: 10.1002/adbi.202400720

Qi Liu, Chunmei Zhang, Yixuan Gao, Dongmei Feng, Duo Deng, Yun Pan

{"title":"Research Progress on the Combination of PARP Inhibitors (PARPi) and Immune Checkpoint Inhibitors (ICIs)","authors":"Qi Liu, Chunmei Zhang, Yixuan Gao, Dongmei Feng, Duo Deng, Yun Pan","doi":"10.1002/adbi.202400720","DOIUrl":"10.1002/adbi.202400720","url":null,"abstract":"Deficiencies in DNA damage repair (DDR), such as poly (ADP-ribose) polymerase (PARP) deficient, cause cancer development by promoting DNA mutations while also exposing the specificity and vulnerability of cancer to afford a treatment option. PARP inhibitor (PARPi) has shown great prospects in the treatment of tumors carrying homologous recombination (HR) deficiencies, such as germline BRCA1/2 mutations. PARPi leads to an increase in the expression of tumor neoantigen, interferon (IFN), and programmed cell death 1/programmed death-ligand 1 (PD-1/PD-L1), which also regulate the tumor microenvironment (TME), promoting a deeper anti-tumor immunotherapy. ICIs targeting PD-1/PD-L1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) have achieved impressive success in the treatment of malignancies. Considering PARPi do enhance the anti-tumor response of ICIs, the combination of PARPi and ICIs has gradually become an alternative treatment option for individuals not receiving apparent efficacy from ICI monotherapy. In this review, the emphasis will be on the mechanisms and immune responses associated with PARPi, profess the principle, then count the clinical studies of this combination therapy.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"9 8","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590228","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

Forskolin Enhances Urokinase Plasminogen Activator Secretion and Angiogenic Activity of Xeno-Free Cultures of Human Adipose Tissue-Derived Stem Cells. Forskolin增强人脂肪组织源性干细胞无xeno培养的尿激酶纤溶酶原激活物分泌和血管生成活性。

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-07-09 DOI: 10.1002/adbi.202400466

Maria Vittoria Giraudo, Anne Therese Lauvrud, Rebecca Wiberg, Maria Brohlin, Gustav Andersson, Paul J Kingham

{"title":"Forskolin Enhances Urokinase Plasminogen Activator Secretion and Angiogenic Activity of Xeno-Free Cultures of Human Adipose Tissue-Derived Stem Cells.","authors":"Maria Vittoria Giraudo, Anne Therese Lauvrud, Rebecca Wiberg, Maria Brohlin, Gustav Andersson, Paul J Kingham","doi":"10.1002/adbi.202400466","DOIUrl":"https://doi.org/10.1002/adbi.202400466","url":null,"abstract":"Adipose tissue-derived stem cells (ASCs) hold significant potential for treating various clinical conditions. To enhance their regenerative properties, ASCs can be chemically stimulated using various in vitro protocols. However, unsatisfactory results persist, partly due to the relatively costly long-term methods. Furthermore, current culturing techniques often rely on the use of xenogenic fetal bovine serum that can be immunogenic, limiting clinical translations. To facilitate clinical translation of ASCs-derived therapeutics, the effect of different stimulation protocols on human ASCs cultured in a xeno-free medium (PRIME-XV MSC Expansion XSFM) is investigated. The xeno-free medium was supplemented with stimulants (forskolin (FSK), basic fibroblast growth factor, platelet-derived growth factor-AA, neuregulin-1) in combinations or individually. Stimulation for 72 h in FSK alone, or together with the growth factors, enhanced the production of urokinase plasminogen activator (uPA), a serine protease involved in tissue remodeling processes. Conditioned medium derived from stimulated ASCs enhanced in vitro angiogenesis and endothelial cells migration. This study shows that pro-angiogenic responses in human ASCs can be enhanced with a defined short stimulation protocol using a xeno-free medium. The protocol, using readily available manufacturing cell therapy grade molecules, may boost the regenerative properties of ASCs secretome which could enhance their efficacy in clinical treatments.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00466"},"PeriodicalIF":3.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590226","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

Modelling Atherosclerotic Plaque Cap Mechanics: Microcalcifications Reduce Mechanical Properties in Mesenchymal Stromal Cell-Based Model. 模拟动脉粥样硬化斑块帽力学：微钙化降低间充质间质细胞模型的力学特性。

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-07-09 DOI: 10.1002/adbi.202500106

Imke L Jansen, Deniz Şahin, Frank J H Gijsen, Eric Farrell, Kim van der Heiden

{"title":"Modelling Atherosclerotic Plaque Cap Mechanics: Microcalcifications Reduce Mechanical Properties in Mesenchymal Stromal Cell-Based Model.","authors":"Imke L Jansen, Deniz Şahin, Frank J H Gijsen, Eric Farrell, Kim van der Heiden","doi":"10.1002/adbi.202500106","DOIUrl":"https://doi.org/10.1002/adbi.202500106","url":null,"abstract":"Rupture of atherosclerotic plaque caps is the cause of many disabling or lethal cardiovascular events, such as stroke and myocardial infarction. Microcalcifications (<50 µm) have been shown, in computational models, to affect the biomechanical stability of the cap. The current study aims to develop a tissue-engineered model of the atherosclerotic fibrous cap with microcalcifications produced by mesenchymal stromal cells (MSCs). Human MSCs are seeded in fibrin gels and cultured for 2 weeks in medium supplemented with TGF-β1 to induce smooth muscle cell differentiation and collagenous matrix formation. Afterward, mineralizing medium stimulates microcalcification formation for an additional 4 weeks. Tissue-engineered structures are imaged after culture with second harmonic generation microscopy with a hydroxyapatite probe, showing collagenous matrix with microcalcifications. Mechanical characterization shows the effect of microcalcifications on global tissue mechanics, as the ultimate stress at rupture of the tissue is significantly lower compared to control tissues. The amount of calcification, determined by histological analysis, is correlated to the decrease in ultimate tensile stress, with a higher amount of microcalcification resulting in weakened mechanical properties. The developed tissue-engineered plaque cap model with biologically formed collagenous matrix and microcalcifications offers valuable insight into the impact of microcalcifications on biomechanical stability.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00106"},"PeriodicalIF":3.2,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590227","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