Biology of the Cell最新文献

{"title":"From Genomic Alterations to Functional Tumor Biology: Integrating Organoids and Organ-on-a-Chip in Colorectal Cancer","authors":"Woei‑Yau Kao,&nbsp;Lu-Kai Wang,&nbsp;Fu-Ming Tsai","doi":"10.1111/boc.70072","DOIUrl":"https://doi.org/10.1111/boc.70072","url":null,"abstract":"<div>\u0000 \u0000 <p>Colorectal cancer (CRC) develops through the stepwise accumulation of genetic alterations, including mutations in <i>APC</i>, <i>KRAS</i>, and <i>TP53</i>, which drive tumor initiation and progression. Although advances in genomic profiling have significantly improved our understanding of CRC, translating these alterations into functional outcomes and therapeutic responses remains a major challenge. This limitation arises from tumor heterogeneity, context-dependent signaling, and the dynamic nature of tumor evolution. Recent advances in patient-derived organoids (PDOs) have provided a platform that preserves tumor-specific architecture and genetic features, enabling functional interrogation of drug responses. However, PDOs lack critical components of the tumor microenvironment, such as stromal, immune, and mechanical cues. Organ-on-a-chip (OoC) technologies, particularly organoid-on-a-chip systems in which PDOs are integrated into microfluidic devices, further address these limitations by recapitulating physiological conditions and multicellular interactions. In this review, we discuss the genetic evolution of CRC and highlight how emerging functional models, including PDOs and organoid-on-a-chip platforms, bridge the gap between genomic alterations and tumor behavior. We propose that integrating these platforms offers a promising framework for advancing functional precision medicine and improving our understanding of CRC biology.</p>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 6","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148306106","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148068369","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148062400","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}

{"title":"Rearrangement of the Cell Chaperone Machinery in Human Fibrosarcoma HT1080 Cells With the Knocked-Out HSP90AA1 Gene Encoding Hsp90α.","authors":"Viktoria Petrenko, Veronika Vrublevskaya, Yuri Skarga, Mariya Zhmurina, Oleg Morenkov","doi":"10.1111/boc.70064","DOIUrl":"10.1111/boc.70064","url":null,"abstract":"<p><strong>Background: </strong>Two isoforms of the 90-kDa heat shock protein (Hsp90), stress-inducible Hsp90α and constitutively expressed Hsp90β, function in mammalian cells as molecular chaperones that promote the folding of specific client proteins involved in essential cellular processes and regulatory pathways. A number of Hsp90 client proteins take part in cancer progression, and the inhibition of Hsp90 induces the degradation of oncogenic client proteins and cancer cell death. Hsp90 inhibitors specific for individual Hsp90 isoforms have a significant potential for the development of anticancer therapeutics due to reduced toxicity. Cells with knocked-out genes encoding Hsp90 isoforms represent excellent cellular models to investigate the rearrangement of the cell chaperone machinery in response to the suppression/loss of the Hsp90 isoforms.</p><p><strong>Results: </strong>Recently, we have shown that the knockout of the HSP90AA1 gene encoding Hsp90α in human fibrosarcoma HT1080 cells does not affect basic cellular processes in normal and stressful conditions, which suggests an adaptation of the cell chaperone machinery to the loss of Hsp90α. Here, we demonstrated that the lack of Hsp90α in HT1080 cells leads to an up-regulation of the constitutively expressed Hsp90β and several important Hsp90 co-chaperones (Aha1, Hop, and others). The expression of the major chaperones of the Hsp70 machinery (Hsp70-1, Hsp70-2, Hsc70) was also significantly induced. The components of the prefoldin-chaperonin folding arm and PFDL, R2TP, and R2SP complexes, as well as the major mitochondrial chaperones, were also largely up-regulated in Hsp90α-KO cells, while the expression of ER-resident chaperones/co-chaperones was either repressed or did not change.</p><p><strong>Conclusions and significance: </strong>We demonstrated here for the first time an adaptation of the cell chaperone machinery to the loss of the Hsp90α chaperone, which may be important for understanding the molecular mechanisms of action of Hsp90α-specific inhibitors and elaborating new therapy strategies in combating cancer, including the combination of Hsp90α-targeted therapy.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":"e70064"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13349343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810390","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}

{"title":"Delta-Cell Area is Unchanged in Human Pregnancy: Evidence From Immunohistochemistry.","authors":"Faheem Seedat, Neva Kandzija, Edward Drydale, Katie Holden, James Bancroft, John A Todd, M Irina Stefana, Manu Vatish","doi":"10.1111/boc.70067","DOIUrl":"10.1111/boc.70067","url":null,"abstract":"<p><strong>Aim: </strong>Pancreatic islet δ-cells produce somatostatin, a paracrine regulator of insulin and glucagon secretion within islets. Although adaptive changes in α- and β-cell populations during pregnancy have been described in both animals and humans, data on δ-cell plasticity are sparse and entirely lacking in human pregnancy. We aimed to determine whether pancreatic islet δ-cell mass undergoes morphological adaptation during human pregnancy.</p><p><strong>Methods and results: </strong>Formalin-fixed paraffin-embedded pancreatic tissue from pregnant (n = 7) and non-pregnant (n = 7) donors was analysed. Sections were immunolabelled for somatostatin to identify δ cells, and whole-slide quantitative analysis was performed using an unbiased automated imaging pipeline. δ-cell area was measured across the entire pancreatic sections and compared between groups. In contrast to previously reported expansion of α- and β-cell populations in pregnancy, δ-cell area was not significantly different between pregnant and non-pregnant donors. No quantitative architectural alterations in δ-cell distribution within islets were observed.</p><p><strong>Conclusion: </strong>Pancreatic δ-cell area does not increase during human pregnancy. These findings demonstrate that endocrine cell plasticity within the maternal pancreas is selective and does not uniformly involve all islet cell subtypes.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":"e70067"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833042","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148103385","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148061860","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}

{"title":"STAT Signaling and Its Anti-Apoptotic Effects in Dehydrated Xenopus laevis.","authors":"Yulia Biggar, Akshay A Kamath, Sarah A Breedon, Kenneth B Storey","doi":"10.1111/boc.70069","DOIUrl":"10.1111/boc.70069","url":null,"abstract":"<p><p>Xenopus laevis survives seasonal droughts by entering a hypometabolic state known as aestivation. One of the mechanisms employed by X. laevis to mitigate aestivation-induced tissue atrophy is gene regulation of pro-survival proteins. We further expand on the role of anti-apoptotic signaling in X. laevis by investigating the effect of signal transducer and activator of transcription (STAT) signaling on downstream anti-apoptotic genes in control and dehydrated liver and skeletal muscle of X. laevis. Herein, we found that STAT signaling is differentially regulated between tissues. STAT3 signaling in the liver and STAT5 signaling in skeletal muscle lead to the selective upregulation of downstream anti-apoptotic proteins. Additionally, pro-apoptotic STAT1 signaling is found to be attenuated in both tissues during dehydration stress. Overall, our results indicate an important role for anti-apoptotic proteins during dehydration stress and their contribution in mitigating aestivation-induced atrophy.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":"e70069"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810392","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148103387","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}

{"title":"Correction to \"Ultrastructure, Polarity, and Reproduction of the Golgi Apparatus\".","authors":"","doi":"10.1111/boc.70065","DOIUrl":"10.1111/boc.70065","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"118 5","pages":"e70065"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760807","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}