Advanced biology最新文献_第9页

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-03-04

引用次数: 0

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-24

引用次数: 0

Dormancy and Recurrence in Breast Cancer Bone Metastasis: From Mechanisms to Clinical Translation 乳腺癌骨转移的休眠与复发：从机制到临床转化。

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-24 DOI: 10.1002/adbi.202500485

Ziqi Sun, Baohong Li, Zichao Chen, Zhen Zhang

{"title":"Dormancy and Recurrence in Breast Cancer Bone Metastasis: From Mechanisms to Clinical Translation","authors":"Ziqi Sun, Baohong Li, Zichao Chen, Zhen Zhang","doi":"10.1002/adbi.202500485","DOIUrl":"10.1002/adbi.202500485","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer bone metastasis often involves a prolonged dormancy phase, during which disseminated tumor cells (DTCs) remain undetectable and resistant to conventional therapies, posing a significant risk for late recurrence. Understanding the underlying mechanisms of tumor dormancy and reactivation is crucial for developing effective clinical interventions. However, current clinical translation faces multiple challenges, including limitations in detecting dormant tumor cells, insufficient biomarkers for dormancy, and difficulties in targeted drug delivery. Recent advances in elucidating the mechanisms of dormancy—such as the establishment of the pre-metastatic niche, intercellular communication in the bone marrow microenvironment, and signaling pathways regulating dormancy and reactivation—have provided novel therapeutic targets. Based on these mechanistic insights, nanotechnology-based drug delivery systems have emerged as promising strategies to precisely target dormant breast cancer cells in bone marrow niches. In this review, we summarize the current understanding of dormancy mechanisms in breast cancer bone metastasis, discuss the barriers hindering clinical translation, and highlight how mechanism-driven nanotherapeutic strategies may offer new opportunities to prevent recurrence by targeting dormant tumor cells.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 2","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281628","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

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-22

引用次数: 0

TWIST1 Activates CDCA3 to Promote EMT of Lung Adenocarcinoma and Expression of PD-L1 TWIST1激活CDCA3促进肺腺癌EMT及PD-L1表达

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-22 DOI: 10.1002/adbi.202500531

Jianyi Ding, Junjun Zhao, Jiandong Zhang, Linhai Fu, Zhupeng Li, Desheng Wei, Guangmao Yu, Haiyong Wang

{"title":"TWIST1 Activates CDCA3 to Promote EMT of Lung Adenocarcinoma and Expression of PD-L1","authors":"Jianyi Ding, Junjun Zhao, Jiandong Zhang, Linhai Fu, Zhupeng Li, Desheng Wei, Guangmao Yu, Haiyong Wang","doi":"10.1002/adbi.202500531","DOIUrl":"10.1002/adbi.202500531","url":null,"abstract":"<div>\u0000 \u0000 <p>CDCA3 and TWIST1 are implicated in cell-cycle control and transcriptional regulation, yet their combined role in lung adenocarcinoma (LUAD) remains unclear. Here, we investigated the impact of the TWIST1/CDCA3 axis on LUAD cell behavior. Leveraging TCGA and KnockTF v2.0, we pinpointed TWIST1 as an upstream driver of CDCA3 in LUAD and delineated associated survival outcomes. ChIP and dual-luciferase assays verified the interaction between CDCA3 and TWIST1. We also quantified CDCA3 and TWIST1 mRNA by qRT-PCR and determined CDCA3, the immune-therapy biomarker PD-L1, and EMT-related protein levels by Western blot. Furthermore, CCK-8, colony formation assays, wound healing, and Transwell assays were conducted to evaluate the malignant behaviors of cells. Bioinformatic and functional analyses revealed that both CDCA3 and TWIST1 were highly expressed in LUAD, and their elevated levels predicted poor prognosis. Further investigation identified TWIST1 as an upstream activator of CDCA3. Knockdown of TWIST1 attenuated the malignant phenotype and reduced PD-L1 expression in LUAD cells, whereas subsequent overexpression of CDCA3 fully reversed these suppressive effects. This study aims to validate that the TWIST1/CDCA3 axis promotes invasion, migration, proliferation, and PD-L1 expression of LUAD cells.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 2","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269441","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

Feiwei Mixture Exerts Antitumor Activity Against Non-Small Cell Lung Cancer via Regulating NR1D1-Mediated Immune Cell Infiltration 飞味合剂通过调节nr1d1介导的免疫细胞浸润对非小细胞肺癌具有抗肿瘤活性。

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-22 DOI: 10.1002/adbi.202500574

Haiyong Wang, Lingsun Guo, Yu Zhao, Jinshu Ye, Tong Zhao, Chufeng Zhang

{"title":"Feiwei Mixture Exerts Antitumor Activity Against Non-Small Cell Lung Cancer via Regulating NR1D1-Mediated Immune Cell Infiltration","authors":"Haiyong Wang, Lingsun Guo, Yu Zhao, Jinshu Ye, Tong Zhao, Chufeng Zhang","doi":"10.1002/adbi.202500574","DOIUrl":"10.1002/adbi.202500574","url":null,"abstract":"<div>\u0000 \u0000 <p>Feiwei Mixture (FWHJ), a hospital preparation for lung cancer, lacks a defined mechanism of action. Using Lewis lung carcinoma (LLC) tumor-bearing mice and an LLC-CD8<sup>+</sup> T cell co-culture model, we evaluated the effects of FWHJ on tumor growth, T cell infiltration, and apoptosis. Key signaling molecules (NR1D1, cGAS-STING, SOCS3-JAK-STAT3) and chemokines were analyzed using Western blot, flow cytometry, and immunoassays. Further knockout of NR1D1 confirmed its critical role in mediating the anti-tumor effects of FWHJ. FWHJ dose-dependently inhibited tumor growth in mice and enhanced CD4<sup>+</sup>/CD8<sup>+</sup> T cell infiltration. It upregulated NR1D1, SOCS3, and the cGAS-STING pathway, while suppressing JAK-STAT3 signaling, leading to increased CCL5, CXCL10, and IFN-α. In co-culture model, FWHJ-containing serum promoted LLC cell apoptosis and suppressed malignant progression, recapitulating the signaling alterations observed in vivo. Crucially, NR1D1 knockout abolished the therapeutic effects of FWHJ. FWHJ inhibits non-small cell lung cancer (NSCLC) by activating NR1D1 to stimulate the cGAS-STING pathway and suppress the JAK-STAT3 signaling axis, thereby enhancing anti-tumor immunity. This study provides a foundation for further investigation into the anti-tumor mechanisms of FWHJ and establishes a scientific basis for its potential application in lung cancer therapy.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 2","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269422","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

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-22

引用次数: 0

Mechanical Dialogues of Life and Death: How External Molecules Entry Triggers a Chromatin-Cytoskeleton Morphogenetic Duel in Cancer Cells 生与死的机械对话：外部分子进入如何触发癌细胞中染色质-细胞骨架形态发生的决斗。

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-19 DOI: 10.1002/adbi.202500716

Parama Dey, Anup Singhania, Ajaikumar B. Kunnumakkara, Subrata Ghosh, Anirban Bandyopadhyay

{"title":"Mechanical Dialogues of Life and Death: How External Molecules Entry Triggers a Chromatin-Cytoskeleton Morphogenetic Duel in Cancer Cells","authors":"Parama Dey, Anup Singhania, Ajaikumar B. Kunnumakkara, Subrata Ghosh, Anirban Bandyopadhyay","doi":"10.1002/adbi.202500716","DOIUrl":"10.1002/adbi.202500716","url":null,"abstract":"<div>\u0000 \u0000 <p>The next-generation anti-cancer therapeutics must disrupt intracellular mechanics, efficiently eradicating cancer cells, rather than simply intoxicating them. We evaluate the mechanism of action of PCMS, a PAMAM-based supramolecule that eradicates cancer cells by reorganizing their internal mechanics rather than their genes. Once internalized, PCMS self-assembles into a perinuclear ring that severs nucleus-cytoskeleton communication. We observed PCMS's dual-intelligent mechanisms of action: Cytoskeletal rescue, where actin-microtubule filaments move towards the PCMS ring, treating it as a surrogate plasma membrane, attempting to restore vesicular trafficking; Nuclear counter-expansion, where chromatin-lamina condensates undergo stepwise viscoelastic transitions that push the nuclear envelope outward to reestablish membrane contact. These contradictory forces amplify mechanical stress, driving super-critical strain and nuclear lysis without broad transcriptional modulations. By geometry alone, PCMS collapses the actin-microtubule-nucleus continuum and turns the cell's adaptive machinery into its own executioner. The discovery that life and death decisions can be reprogrammed through spatial conflict establishes a paradigm of mechanical deception, inaugurating a new class of cellular adaptive feedback-targeted mechanotherapeutics that overcome resistance by exploiting the cell's own morphogenetic logic.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 2","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146224833","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

Mechanical Cues and Lineage Commitment Govern the Angiogenic Potential of Mesenchymal Cell-Derived Extracellular Vesicles 机械提示和谱系承诺控制间充质细胞衍生的细胞外囊泡的血管生成潜能。

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-19 DOI: 10.1002/adbi.202500544

Carolina S. Martins, Mimma Maggio, Cansu Gorgun, Mathieu Y. Brunet, Marko Dobricic, R. Almasri, Fergal J. O'Brien, Lorraine O'Driscoll, David A. Hoey

{"title":"Mechanical Cues and Lineage Commitment Govern the Angiogenic Potential of Mesenchymal Cell-Derived Extracellular Vesicles","authors":"Carolina S. Martins, Mimma Maggio, Cansu Gorgun, Mathieu Y. Brunet, Marko Dobricic, R. Almasri, Fergal J. O'Brien, Lorraine O'Driscoll, David A. Hoey","doi":"10.1002/adbi.202500544","DOIUrl":"10.1002/adbi.202500544","url":null,"abstract":"<p>Bone regeneration requires a finely tuned interplay between osteogenesis and angiogenesis. While current treatments, such as auto/allografts, provide support, they often fail to promote adequate vascularization necessary for complete repair. Extracellular vesicles (EVs), as mediators of intercellular communication, have emerged as promising acellular nanotechnologies for tissue regeneration due to their bioactive cargo and low immunogenicity. Mechanical stimulation, a known enhancer of bone cell function, can modulate EV cargo and potentially improve regenerative efficacy. In this study, we investigated how mechanical stimulation and the stage of mesenchymal lineage commitment influence the angiogenic potential of secretomes and EVs derived from mesenchymal stromal/stem cells, osteoblasts, and osteocytes. Our findings reveal that both cell mechanical stimulation and their differentiation stage significantly modulate the angiogenic properties of the resulting EVs. Among the tested conditions, mechanically-stimulated osteocyte-derived EVs demonstrate superior angiogenesis, promoting endothelial cell migration, tube formation, and CD31 expression. These effects were further validated in a pre-clinical ex ovo chick chorioallantoic membrane assay, where robust neovascularization was observed. This work highlights the critical role of both mechanical cues and cell differentiation stage in regulating the angiogenic capacity of EVs and proposes mechanically activated osteocyte-derived EVs as a novel pro-angiogenic nanotherapeutic for bone repair.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 2","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12921385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146224868","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

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-02-19

引用次数: 0