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Turning end-joining upside down in mitosis 有丝分裂中的翻转末端连接
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2007029
M. Llorens-Agost, M. Ensminger, H. Le, W. Heyer, M. Löbrich
{"title":"Turning end-joining upside down in mitosis","authors":"M. Llorens-Agost, M. Ensminger, H. Le, W. Heyer, M. Löbrich","doi":"10.1080/23723556.2021.2007029","DOIUrl":"https://doi.org/10.1080/23723556.2021.2007029","url":null,"abstract":"ABSTRACT How cells deal with DNA breaks during mitosis is not well understood. While canonical non-homologous end-joining predominates in interphase, it is inhibited in mitosis to avoid telomere fusions. DNA polymerase θ mediated end-joining appears to be repressed in interphase, but promotes break repair in mitosis. The nature and induction time of breaks might determine their fate during mitosis.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46518080","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
Mitotic WNT: aligning chromosomes through KIF2A 有丝分裂WNT：通过KIF2A排列染色体
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2011564
A. Bufe, S. Acebrón
{"title":"Mitotic WNT: aligning chromosomes through KIF2A","authors":"A. Bufe, S. Acebrón","doi":"10.1080/23723556.2021.2011564","DOIUrl":"https://doi.org/10.1080/23723556.2021.2011564","url":null,"abstract":"ABSTRACT WNT signaling regulates cell cycle progression and fate determination through β-catenin dependent transcription, and its misregulation is often associated with tumorigenesis. Our recent work demonstrated that basal WNT activity is also required to ensure proper chromosome alignment during mitosis through the regulation of kinesin family member 2A (KIF2A).","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42293068","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
KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma. KMT2D缺陷赋予黑色素瘤对糖酵解和IGFR抑制剂的治疗脆弱性。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-11-01 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1984827
Navya Murugesan, Mayinuer Maitituoheti
{"title":"<i>KMT2D</i> deficiency confers a therapeutic vulnerability to glycolytic and <i>IGFR</i> inhibitors in melanoma.","authors":"Navya Murugesan,&nbsp;Mayinuer Maitituoheti","doi":"10.1080/23723556.2021.1984827","DOIUrl":"https://doi.org/10.1080/23723556.2021.1984827","url":null,"abstract":"<p><p>We reported that histone H3 lysine (K) 4 methyltransferase, <i>KMT2D</i>, serves as a potent tumor-suppressor in melanoma, which was identified via <i>in vivo</i> epigenome-focused RNA interference (RNAi) screen. <i>KMT2D</i>-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1984827"},"PeriodicalIF":2.1,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/30/KMCO_8_1984827.PMC8632269.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39687923","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
ERBB3 as a therapeutic target in glioblastoma: overexpression can make the difference. ERBB3作为胶质母细胞瘤的治疗靶点:过表达会产生差异。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1990677
Francesca De Bacco, Carla Boccaccio
{"title":"ERBB3 as a therapeutic target in glioblastoma: overexpression can make the difference.","authors":"Francesca De Bacco,&nbsp;Carla Boccaccio","doi":"10.1080/23723556.2021.1990677","DOIUrl":"https://doi.org/10.1080/23723556.2021.1990677","url":null,"abstract":"ABSTRACT By exploiting an integrated experimental platform based on patient-derived cancer stem cells, we identified a glioblastoma subset characterized by inheritable Erb-B2 Receptor Tyrosine Kinase 3 (ERBB3) overexpression, metabolic dependency on ERBB3 signaling, and liability to ERBB3 targeting. We provide insights on why some glioblastomas may rely on ERBB3 and how to recognize them.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1990677"},"PeriodicalIF":2.1,"publicationDate":"2021-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b2/a3/KMCO_8_1990677.PMC8632286.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39687927","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
Targeting cancer’s sweet spot: UGP2 as a therapeutic vulnerability 靶向癌症的最佳点:作为治疗弱点的UGP2
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-27 DOI: 10.1080/23723556.2021.1990676
Sunghoon Kim, A. Wolfe, S. Kim
{"title":"Targeting cancer’s sweet spot: UGP2 as a therapeutic vulnerability","authors":"Sunghoon Kim, A. Wolfe, S. Kim","doi":"10.1080/23723556.2021.1990676","DOIUrl":"https://doi.org/10.1080/23723556.2021.1990676","url":null,"abstract":"ABSTRACT Understanding the mechanisms governing metabolic reprogramming that underlie potential vulnerabilities in cancer cells is key to developing novel therapeutic strategies. The catalytic enzyme UDP-glucose pyrophosphorylase 2 (UGP2) drives the production of UDP-glucose. Our recent work demonstrated the crucial role of UGP2 in cancer growth and its regulation of cellular metabolic processes.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43144158","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
Targeting the immune microenvironment during immunotherapy for solid tumors. 实体肿瘤免疫治疗中的免疫微环境靶向。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1994327
Aiman Sabaawy, Saman Zeeshan
{"title":"Targeting the immune microenvironment during immunotherapy for solid tumors.","authors":"Aiman Sabaawy,&nbsp;Saman Zeeshan","doi":"10.1080/23723556.2021.1994327","DOIUrl":"https://doi.org/10.1080/23723556.2021.1994327","url":null,"abstract":"<p><p>JAK/STAT signaling is a central hub in cancer development, progression, immunosurveillance and response to immunotherapy. We discuss recent advances in the role of the JAK/STAT pathway in immunotherapies. We stress the importance of fully understanding how JAK/STAT modifies the immune response before implementing clinical trials combining JAK/STAT inhibitors with immunotherapy.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1994327"},"PeriodicalIF":2.1,"publicationDate":"2021-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632277/pdf/KMCO_8_1994327.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39688331","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: 3
Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS-mutant melanoma. 染色质状态分析揭示PRC2抑制是nras突变黑色素瘤的治疗靶点。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1986350
Christopher J Terranova
{"title":"Chromatin state profiling reveals PRC2 inhibition as a therapeutic target in NRAS-mutant melanoma.","authors":"Christopher J Terranova","doi":"10.1080/23723556.2021.1986350","DOIUrl":"https://doi.org/10.1080/23723556.2021.1986350","url":null,"abstract":"<p><p>Recently, we have generated 284 epigenomic maps in melanoma. Using chromatin state profiling we identify an association of <i>NRAS</i>-mutants with bivalent Histone H3 lysine 27 trimethylation (H3K27me3) and broad H3K4me3 domains. Reprogramming of bivalent H3K27me3 occurs on critical invasive-regulators and its resolution using Enhancer of Zeste Homolog 2 (EZH2) inhibition reduces invasive capacity and tumor burden in <i>NRAS-</i>mutant patient samples.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1986350"},"PeriodicalIF":2.1,"publicationDate":"2021-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/53/d9/KMCO_8_1986350.PMC8632323.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39687925","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
Dedifferentiation of esophageal progenitors in metaplasia and cancer 化生和癌中食管祖细胞的去分化
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-21 DOI: 10.1080/23723556.2021.1991758
Alizée Vercauteren Drubbel, Benjamin Beck
{"title":"Dedifferentiation of esophageal progenitors in metaplasia and cancer","authors":"Alizée Vercauteren Drubbel, Benjamin Beck","doi":"10.1080/23723556.2021.1991758","DOIUrl":"https://doi.org/10.1080/23723556.2021.1991758","url":null,"abstract":"ABSTRACT Barrett syndrome is a squamo-columnar metaplasia increasing the risk of developing esophageal adenocarcinoma. Recently, we showed that esophageal cells can transdifferentiate into undifferentiated columnar cells in vivo. Here, we discuss about the potential of these cells to be a reservoir for intestinal metaplasia and/or esophageal adenocarcinoma.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43520936","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
How multi-component cascades operate in cells: lessons from the ubiquitin system-containing liquid-separated condensates. 多组分级联如何在细胞中运作:来自泛素系统含液体分离凝聚物的教训。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-21 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1989939
Afu Fu, Ido Livneh, Aaron Ciechanover, Victoria Cohen-Kaplan
{"title":"How multi-component cascades operate in cells: lessons from the ubiquitin system-containing liquid-separated condensates.","authors":"Afu Fu,&nbsp;Ido Livneh,&nbsp;Aaron Ciechanover,&nbsp;Victoria Cohen-Kaplan","doi":"10.1080/23723556.2021.1989939","DOIUrl":"https://doi.org/10.1080/23723556.2021.1989939","url":null,"abstract":"<p><p>Membraneless condensates have recently caught the attention of biologists as hubs for cellular components required for catalysis of basic processes. Whether they are real has become the center of heated discussion where the main issues are their mechanism of assembly and function. A recent study describing these condensates as hubs for protein degradation by the ubiquitin system may shed a new light on this recent development in cell biology.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1989939"},"PeriodicalIF":2.1,"publicationDate":"2021-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632267/pdf/KMCO_8_1989939.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39687926","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
Adipose stromal cells promote the transition of colorectal cancer cells toward a mesenchymal-like phenotype. 脂肪间质细胞促进结直肠癌细胞向间充质样表型转变。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-10-18 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1986343
Simone Di Franco, Giorgio Stassi
{"title":"Adipose stromal cells promote the transition of colorectal cancer cells toward a mesenchymal-like phenotype.","authors":"Simone Di Franco,&nbsp;Giorgio Stassi","doi":"10.1080/23723556.2021.1986343","DOIUrl":"https://doi.org/10.1080/23723556.2021.1986343","url":null,"abstract":"<p><p>Colon cancer progression is among the risks that increase with obesity. We have recently unveiled the molecular mechanism by which adipose tissue-released molecules, HGF and IL-6, make colorectal cancer (CRC) cells acquiring mesenchymal traits. Targeting of adipose-derived factors abrogate the metastatic potential of CRC stem cells (CR-CSCs) in obese patients.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1986343"},"PeriodicalIF":2.1,"publicationDate":"2021-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ec/ea/KMCO_8_1986343.PMC8632327.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39687924","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
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