Molecular & cellular oncology最新文献

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A perspective on DNA damage-induced potentiation of the pentose phosphate shunt and reductive stress in chemoresistance. DNA损伤诱导的戊糖磷酸分流增强和化学抗性还原性应激的研究进展。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-22 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1733383
Chiara Milanese, Pier G Mastroberardino
{"title":"A perspective on DNA damage-induced potentiation of the pentose phosphate shunt and reductive stress in chemoresistance.","authors":"Chiara Milanese,&nbsp;Pier G Mastroberardino","doi":"10.1080/23723556.2020.1733383","DOIUrl":"https://doi.org/10.1080/23723556.2020.1733383","url":null,"abstract":"<p><p>Metabolic rearrangements and genome instability are two hallmarks of cancer. Recent evidence from our laboratory demonstrates that persistent DNA lesions hampering transcription may cause glucose rerouting through the pentose phosphate shunt and reductive stress. Here, we highlight the relevance of these findings for cancer and chemoresistance development.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1733383"},"PeriodicalIF":2.1,"publicationDate":"2020-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1733383","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922232","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
Ferroptosis resistance mediated by exosomal release of iron. 铁的外泌体释放介导的铁下垂抗性。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-21 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1730144
Caitlin W Brown, Arthur M Mercurio
{"title":"Ferroptosis resistance mediated by exosomal release of iron.","authors":"Caitlin W Brown,&nbsp;Arthur M Mercurio","doi":"10.1080/23723556.2020.1730144","DOIUrl":"https://doi.org/10.1080/23723556.2020.1730144","url":null,"abstract":"<p><p>Understanding how cells resist ferroptosis is necessary for exploiting this iron-dependent mode of cell death for the treatment of cancer and other diseases. We discovered that cells resist ferroptosis by enabling a PROMININ2-dependent iron export pathway involving multivesicular body/exosome trafficking of iron out of the cell, diminishing the intracellular iron needed for ferroptosis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1730144"},"PeriodicalIF":2.1,"publicationDate":"2020-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1730144","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922231","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: 10
Lysine succinylation and SIRT5 couple nutritional status to glutamine catabolism. 赖氨酸琥珀酰化和SIRT5将营养状况与谷氨酰胺分解代谢联系起来。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-19 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1735284
Michael J Lukey, Kai Su Greene, Richard A Cerione
{"title":"Lysine succinylation and SIRT5 couple nutritional status to glutamine catabolism.","authors":"Michael J Lukey,&nbsp;Kai Su Greene,&nbsp;Richard A Cerione","doi":"10.1080/23723556.2020.1735284","DOIUrl":"https://doi.org/10.1080/23723556.2020.1735284","url":null,"abstract":"<p><p>The metabolic microenvironment of tumors is characterized by fluctuating and limited nutrient availability. To survive these conditions, cancer cell-intrinsic mechanisms sense and signal nutritional status. We describe how glutaminase (GLS) is destabilized by lysine succinylation and stabilized by the NAD<sup>+</sup>-dependent desuccinylase sirtuin 5 (SIRT5), coupling nutrient levels to metabolic flux.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1735284"},"PeriodicalIF":2.1,"publicationDate":"2020-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1735284","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922233","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: 7
A novel role for TTK in homologous recombination: implications for breast cancer radiosensitivity. TTK在同源重组中的新作用:对乳腺癌放射敏感性的影响。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-19 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1737771
Benjamin C Chandler, Corey Speers
{"title":"A novel role for TTK in homologous recombination: implications for breast cancer radiosensitivity.","authors":"Benjamin C Chandler,&nbsp;Corey Speers","doi":"10.1080/23723556.2020.1737771","DOIUrl":"https://doi.org/10.1080/23723556.2020.1737771","url":null,"abstract":"<p><p>Basal-like breast cancers have the highest rates of locoregional recurrence after radiation. By correlating gene expression with early locoregional recurrence, we nominate TTK protein kinase as a mediator of radioresistance. TTK inhibition radiosensitizes <i>in vitro</i> and <i>in vivo</i> through a novel mechanism of impaired homologous recombination and represents a promising translational strategy.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1737771"},"PeriodicalIF":2.1,"publicationDate":"2020-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1737771","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922194","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: 2
Mitotic stress-induced secretome primes cancer cells to apoptosis and maximizes paclitaxel response in breast tumors when combined with BCL-xL-targeting BH3 mimetics. 当与靶向bcl - xl的BH3模拟物联合使用时,有丝分裂应激诱导的分泌组诱导癌细胞凋亡并最大化紫杉醇反应。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-19 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1735912
Steven Lohard, Philippe P Juin, Sophie Barillé-Nion
{"title":"Mitotic stress-induced secretome primes cancer cells to apoptosis and maximizes paclitaxel response in breast tumors when combined with BCL-xL-targeting BH3 mimetics.","authors":"Steven Lohard,&nbsp;Philippe P Juin,&nbsp;Sophie Barillé-Nion","doi":"10.1080/23723556.2020.1735912","DOIUrl":"https://doi.org/10.1080/23723556.2020.1735912","url":null,"abstract":"<p><p>We recently identified a previously unappreciated ability of antimitotics to propagate apoptotic priming across cancer cell populations. The underlying paracrine cytotoxic signal, fueled by undead cells activating the cGAS/STING pathway, is required for in vivo antitumor response and it can be further exploited by delayed, but not synchronous, BCL-xL inhibition.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1735912"},"PeriodicalIF":2.1,"publicationDate":"2020-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1735912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922236","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
Complexities of pharmacogenomic interactions in cancer. 癌症中药物基因组相互作用的复杂性。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-19 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1735910
Kum Kum Khanna, Pascal H G Duijf
{"title":"Complexities of pharmacogenomic interactions in cancer.","authors":"Kum Kum Khanna,&nbsp;Pascal H G Duijf","doi":"10.1080/23723556.2020.1735910","DOIUrl":"https://doi.org/10.1080/23723556.2020.1735910","url":null,"abstract":"<p><p>Genetic and genomic alterations drive cancer development. However, they may also constitute vulnerabilities, including increased drug sensitivity, which could be harnessed for precision medicine purposes. We discuss the highly complex pharmacogenomic interactions that are beginning to be disentangled and hurdles that may need to be overcome before cancer patients could benefit.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1735910"},"PeriodicalIF":2.1,"publicationDate":"2020-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1735910","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922234","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: 4
Targeting the oncogenic activity of TCF3-HLF in leukemia. 靶向TCF3-HLF在白血病中的致瘤活性。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-18 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2019.1709391
Yun Huang, Jean-Pierre Bourquin
{"title":"Targeting the oncogenic activity of TCF3-HLF in leukemia.","authors":"Yun Huang,&nbsp;Jean-Pierre Bourquin","doi":"10.1080/23723556.2019.1709391","DOIUrl":"https://doi.org/10.1080/23723556.2019.1709391","url":null,"abstract":"<p><p>The oncogenic fusion transcription factor TCF3-HLF identifies an aggressive subtype of acute lymphoblastic leukemia. TCF3-HLF imposes a malignant program by activation of lineage-specific oncogenic enhancers. Among critical cofactors of the TCF3-HLF complex we identified EP300, which functional inhibition results in potent anti-leukemic activity by interference with the specific gene expression.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1709391"},"PeriodicalIF":2.1,"publicationDate":"2020-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2019.1709391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37921790","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: 4
PBRM1 suppresses tumor growth as a novel p53 acetylation reader. PBRM1作为一种新的p53乙酰化解读器抑制肿瘤生长。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-11 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1729680
Weijia Cai, Liya Su, Haifeng Yang
{"title":"PBRM1 suppresses tumor growth as a novel p53 acetylation reader.","authors":"Weijia Cai,&nbsp;Liya Su,&nbsp;Haifeng Yang","doi":"10.1080/23723556.2020.1729680","DOIUrl":"https://doi.org/10.1080/23723556.2020.1729680","url":null,"abstract":"<p><p>The reader(s) for acetylated tumor antigen p53 remains elusive. Here, PBRM1 (polybromo-1) is identified as a reader for acetylated lysine382 on p53 through its bromodomain 4 (BD4). <i>PBRM1</i> BD4 mutants fail to support p53 transcriptional activity and suppress tumor growth. Thus PBRM1 suppresses tumor growth through p53 in kidney cancer.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1729680"},"PeriodicalIF":2.1,"publicationDate":"2020-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1729680","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922229","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: 2
Emerging role of mRNA epitranscriptomic regulation in chemoresistant cancer cells. mRNA表转录组调控在化疗耐药癌细胞中的新作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-09 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1728467
Shensi Shen, Xiaoxiao Sun
{"title":"Emerging role of mRNA epitranscriptomic regulation in chemoresistant cancer cells.","authors":"Shensi Shen,&nbsp;Xiaoxiao Sun","doi":"10.1080/23723556.2020.1728467","DOIUrl":"https://doi.org/10.1080/23723556.2020.1728467","url":null,"abstract":"<p><p>Cancer persister cells remain a significant barrier to effective anti-cancer therapy. We found that melanoma persister cells undergo a reversible reprogramming of mRNA translation. A subset of mRNAs, harboring N6-methyladenosine in their 5'-untranslated regions, is translationally up-regulated in an eIF4A-dependent manner. Targeting eIF4A prevents the emergence of resistant clones.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1728467"},"PeriodicalIF":2.1,"publicationDate":"2020-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1728467","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922228","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
Axin2+ endometrial stem cells: the source of endometrial regeneration and cancer. Axin2+子宫内膜干细胞:子宫内膜再生和癌症的来源。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-03-05 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1729681
Shafiq M Syed, Pradeep S Tanwar
{"title":"Axin2<sup>+</sup> endometrial stem cells: the source of endometrial regeneration and cancer.","authors":"Shafiq M Syed,&nbsp;Pradeep S Tanwar","doi":"10.1080/23723556.2020.1729681","DOIUrl":"https://doi.org/10.1080/23723556.2020.1729681","url":null,"abstract":"<p><p>Menstruation is one of the basic but poorly understood life processes in primates during which females shed inner uterine lining every month only to be completely regenerated back within a week. The definitive evidence for the existence and/or identity of stem cells responsible for this process has remained elusive for more than six decades now. Recently, we reported Axin2, a classical Wnt reporter gene, as a marker for endometrial stem cells that also serve as the cells of origin for endometrial cancer.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1729681"},"PeriodicalIF":2.1,"publicationDate":"2020-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1729681","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922230","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: 7
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