Advances in biological regulation最新文献_第10页

Modified lipidomic profile of cancer-associated small extracellular vesicles facilitates tumorigenic behaviours and contributes to disease progression 癌症相关的细胞外小泡的脂质组学特征的改变促进了致瘤行为并有助于疾病进展

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100935

Jordan Fyfe, Pratibha Malhotra, Marco Falasca

引用次数: 1

PIP kinases: A versatile family that demands further therapeutic attention PIP激酶:一个多功能家族，需要进一步的治疗关注

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100939

Alicia Llorente, Gurpreet K. Arora , Shea F. Grenier , Brooke M. Emerling

引用次数: 1

From form to function: m6A methylation links mRNA structure to metabolism 从形式到功能：m6A甲基化将mRNA结构与代谢联系起来

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100926

Braulio Martinez De La Cruz, Marousa Darsinou, Antonella Riccio

引用次数: 1

Key to photograph of participants 参加者照片的钥匙

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100952

引用次数: 0

Phospholipase D and cancer metastasis: A focus on exosomes 磷脂酶D与肿瘤转移:以外泌体为中心

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100924

Alexander Wolf, Emeline Tanguy, Qili Wang, Stéphane Gasman, Nicolas Vitale

{"title":"Phospholipase D and cancer metastasis: A focus on exosomes","authors":"Alexander Wolf, Emeline Tanguy, Qili Wang, Stéphane Gasman, Nicolas Vitale","doi":"10.1016/j.jbior.2022.100924","DOIUrl":"10.1016/j.jbior.2022.100924","url":null,"abstract":"<div><p>In mammals, phospholipase D (PLD) enzymes involve 6 isoforms, of which only three have established lipase activity to produce the signaling lipid phosphatidic acid (PA). This phospholipase activity has been postulated to contribute to cancer progression for over three decades now, but the exact mechanisms involved have yet to be uncovered. Indeed, using various models, an altered PLD activity has been proposed altogether to increase cell survival rate, promote angiogenesis, boost rapamycin resistance, and favor metastasis. Although for some part, the molecular pathways by which this increase in PA is pro-oncogenic are partially known, the pleiotropic functions of PA make it quite difficult to distinguish which among these simple signaling pathways is responsible for each of these PLD facets. In this review, we will describe an additional potential contribution of PA generated by PLD1 and PLD2 in the biogenesis, secretion, and uptake of exosomes. Those extracellular vesicles are now viewed as membrane vehicles that carry informative molecules able to modify the fate of receiving cells at distance from the original tumor to favor homing of metastasis. The perspectives for a better understanding of these complex role of PLDs will be discussed.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100924"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9173474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Advances in MDS/AML and inositide signalling MDS/AML和肌苷信号传导的研究进展

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2023.100955

Alessia De Stefano , Maria Vittoria Marvi , Antonietta Fazio , James A. McCubrey , Pann-Ghill Suh , Stefano Ratti , Giulia Ramazzotti , Lucia Manzoli , Lucio Cocco , Matilde Y. Follo

引用次数: 1

Flimsy Overlay 脆弱的叠加

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100951

引用次数: 0

The mutational profiles and corresponding therapeutic implications of PI3K mutations in cancer 癌症中PI3K突变的突变谱及其相应的治疗意义

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100934

Nathan K. VanLandingham , Andrew Nazarenko , Jennifer R. Grandis , Daniel E. Johnson

{"title":"The mutational profiles and corresponding therapeutic implications of PI3K mutations in cancer","authors":"Nathan K. VanLandingham , Andrew Nazarenko , Jennifer R. Grandis , Daniel E. Johnson","doi":"10.1016/j.jbior.2022.100934","DOIUrl":"10.1016/j.jbior.2022.100934","url":null,"abstract":"<div><p>Genetic alterations of the <em>PIK3CA</em> gene, encoding the p110α catalytic subunit of PI3Kα enzyme, are found in a broad spectrum of human cancers. Many cancer-associated <em>PIK3CA</em> mutations occur at 3 hotspot locations and are termed canonical mutations. Canonical mutations result in hyperactivation of PI3K and promote oncogenesis via the PI3K/AKT/mTOR and PI3K/COX-2/PGE2 signaling pathways. These mutations also may serve as predictive biomarkers of response to PI3K inhibitors, as well as NSAID therapy. A large number of non-canonical <em>PIK3CA</em> mutations have also been identified in human tumors, but their functional properties are poorly understood. Here we review the landscape of <em>PIK3CA</em> mutations in different cancers and efforts underway to define the functional properties of non-canonical <em>PIK3CA</em> mutations. In addition, we summarize what has been learned from clinical trials of PI3K inhibitors as well as current trials incorporating these molecular targeting agents.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100934"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9992323/pdf/nihms-1873733.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9525297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AP-4 loss in CRISPR-edited zebrafish affects early embryo development crispr编辑的斑马鱼AP-4缺失影响早期胚胎发育

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100945

Olivia G. Pembridge , Natalie S. Wallace , Thomas P. Clements , Lauren P. Jackson

{"title":"AP-4 loss in CRISPR-edited zebrafish affects early embryo development","authors":"Olivia G. Pembridge , Natalie S. Wallace , Thomas P. Clements , Lauren P. Jackson","doi":"10.1016/j.jbior.2022.100945","DOIUrl":"10.1016/j.jbior.2022.100945","url":null,"abstract":"<div><p>Mutations in the heterotetrametric adaptor protein 4 (AP-4; ε/β4/μ4/σ4 subunits) membrane trafficking coat complex lead to complex neurological disorders characterized by spastic paraplegia, microcephaly, and intellectual disabilities. Understanding molecular mechanisms underlying these disorders continues to emerge with recent identification of an essential autophagy protein, ATG9A, as an AP-4 cargo. Significant progress has been made uncovering AP-4 function in cell culture and patient-derived cell lines, and ATG9A trafficking by AP-4 is considered a potential target for gene therapy approaches. In contrast, understanding how AP-4 trafficking affects development and function at the organismal level has long been hindered by loss of conserved AP-4 genes in key model systems (<em>S. cerevisiae</em>, <em>C. elegans</em>, <em>D. melanogaster</em>). However, zebrafish (<em>Danio rerio</em>) have retained AP-4 and can serve as an important model system for studying both the nervous system and overall development. We undertook gene editing in zebrafish using a CRISPR-ExoCas9 knockout system to determine how loss of single AP-4, or its accessory protein tepsin, genes affect embryo development 24 h post-fertilization (hpf). Single gene-edited embryos display abnormal head morphology and neural necrosis. We further conducted the first exploration of how AP-4 single gene knockouts in zebrafish embryos affect expression levels and patterns of two autophagy genes, <em>atg9a</em> and <em>map1lc3b</em>. This work suggests zebrafish may be further adapted and developed as a tool to uncover AP-4 function in membrane trafficking and autophagy in the context of a model organism.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100945"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9992121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9174139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Silencing effects of mutant RAS signalling on transcriptomes 突变体RAS信号对转录组的沉默作用

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100936

Christine Sers , Reinhold Schäfer

{"title":"Silencing effects of mutant RAS signalling on transcriptomes","authors":"Christine Sers , Reinhold Schäfer","doi":"10.1016/j.jbior.2022.100936","DOIUrl":"10.1016/j.jbior.2022.100936","url":null,"abstract":"<div><p>Mutated genes of the RAS family encoding small GTP-binding proteins drive numerous cancers, including pancreatic, colon and lung tumors. Besides the numerous effects of mutant RAS gene expression on aberrant proliferation, transformed phenotypes, metabolism, and therapy resistance, the most striking consequences of chronic RAS activation are changes of the genetic program. By performing systematic gene expression studies in cellular models that allow comparisons of pre-neoplastic with RAS-transformed cells, we and others have estimated that 7 percent or more of all transcripts are altered in conjunction with the expression of the oncogene. In this context, the number of up-regulated transcripts approximates that of down-regulated transcripts. While up-regulated transcription factors such as MYC, FOSL1, and HMGA2 have been identified and characterized as RAS-responsive drivers of the altered transcriptome, the suppressed factors have been less well studied as potential regulators of the genetic program and transformed phenotype in the breadth of their occurrence. We therefore have collected information on downregulated RAS-responsive factors and discuss their potential role as tumor suppressors that are likely to antagonize active cancer drivers. To better understand the active mechanisms that entail anti-RAS function and those that lead to loss of tumor suppressor activity, we focus on the tumor suppressor HREV107 (alias PLAAT3 [Phospholipase A and acyltransferase 3], PLA2G16 [Phospholipase A2, group XVI] and HRASLS3 [HRAS-like suppressor 3]). Inactivating HREV107 mutations in tumors are extremely rare, hence epigenetic causes modulated by the RAS pathway are likely to lead to down-regulation and loss of function.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100936"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9173956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0