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A mTORC1-mediated cyst(e)ine sensing mechanism governing GPX4 synthesis and ferroptosis. mtorc1介导的囊肿(e)线感应机制调控GPX4合成和铁凋亡。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-27 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1919006
Yuelong Yan, Guang Lei, Boyi Gan
{"title":"A mTORC1-mediated cyst(e)ine sensing mechanism governing GPX4 synthesis and ferroptosis.","authors":"Yuelong Yan,&nbsp;Guang Lei,&nbsp;Boyi Gan","doi":"10.1080/23723556.2021.1919006","DOIUrl":"https://doi.org/10.1080/23723556.2021.1919006","url":null,"abstract":"<p><p>Ferroptosis is a cell death mechanism triggered by lipid peroxidation. Our recent study linked cyst(e)ine availability with glutathione peroxidase 4 (GPX4) protein synthesis and ferroptosis mitigation via a Rag-mechanistic target of rapamycin complex 1 (mTORC1) axis, and proposed that co-targeting mTORC1 and ferroptosis is a promising strategy for cancer therapy.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1919006"},"PeriodicalIF":2.1,"publicationDate":"2021-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1919006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39012050","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
HDAC2 links ubiquitination to tumor suppression in synovial sarcoma. HDAC2将泛素化与滑膜肉瘤的肿瘤抑制联系起来。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-25 DOI: 10.1080/23723556.2021.1914291
Christina Cooley, Le Su
{"title":"HDAC2 links ubiquitination to tumor suppression in synovial sarcoma.","authors":"Christina Cooley,&nbsp;Le Su","doi":"10.1080/23723556.2021.1914291","DOIUrl":"https://doi.org/10.1080/23723556.2021.1914291","url":null,"abstract":"<p><p>The function of histone deacetylase 2 (HDAC2) in transcriptional regulation and its role in oncogenesis have been well established. Here we discuss a transcription-independent HDAC2 pathway controlling cancer-related protein stability via the mouse double minute 2 homolog (MDM2) ubiquitin ligase. In synovial sarcoma, HDAC2 inactivation demonstrates significant therapeutic effect by degradation of the SS18-SSX driver oncoprotein.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1914291"},"PeriodicalIF":2.1,"publicationDate":"2021-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1914291","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39012047","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: 5
Relevance of aneuploidy for cancer therapies targeting the spindle assembly checkpoint and KIF18A. 非整倍性与针对纺锤体组装检查点和KIF18A的癌症治疗的相关性。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-25 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1915075
Yael Cohen-Sharir, Uri Ben-David
{"title":"Relevance of aneuploidy for cancer therapies targeting the spindle assembly checkpoint and KIF18A.","authors":"Yael Cohen-Sharir,&nbsp;Uri Ben-David","doi":"10.1080/23723556.2021.1915075","DOIUrl":"https://doi.org/10.1080/23723556.2021.1915075","url":null,"abstract":"<p><p>Aneuploidy, a common feature of cancer cells, results in increased sensitivity to the inhibition of the spindle assembly checkpoint (SAC) and the mitotic motor protein Kinesin Family Member 18A (KIF18A). We discuss the importance of drugs targeting SAC core members and KIF18A. We stress the need to assess the sensitivity to this class of drugs at appropriate time points, and propose that aneuploidy could serve as a biomarker to stratify patients for SAC-targeting treatments.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1915075"},"PeriodicalIF":2.1,"publicationDate":"2021-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1915075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39012048","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
Unlocking p53 response elements: DNA shape is the key. 解锁p53反应要素:DNA形状是关键。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-22 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1905489
Marina Farkas, Steven McMahon
{"title":"Unlocking p53 response elements: DNA shape is the key.","authors":"Marina Farkas,&nbsp;Steven McMahon","doi":"10.1080/23723556.2021.1905489","DOIUrl":"https://doi.org/10.1080/23723556.2021.1905489","url":null,"abstract":"<p><p>For recognition of specific regulatory sequences in the genome (i.e., response elements, REs), the tumor suppressor protein 53 kDa (p53) exhibits dose-dependent selectivity. In general, binding to REs linked to target genes involved in the positive regulation of cell death requires higher levels of p53 than those connected to cell survival. Our recent findings provide a mechanistic explanation for this phenomenon. Specifically, we demonstrate that subtle differences in DNA shape, encoded in RE DNA sequence, determine the utilization of two biochemically distinct DNA-binding modes, ultimately connected to different biological outcomes.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1905489"},"PeriodicalIF":2.1,"publicationDate":"2021-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1905489","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010565","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
New link between the RNA polymerase II-CTD and replication stress. RNA聚合酶II-CTD与复制应激之间的新联系。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-18 DOI: 10.1080/23723556.2021.1910008
Helga B Landsverk, Lise E Sandquist, Lilli T E Bay, Randi G Syljuåsen
{"title":"New link between the RNA polymerase II-CTD and replication stress.","authors":"Helga B Landsverk,&nbsp;Lise E Sandquist,&nbsp;Lilli T E Bay,&nbsp;Randi G Syljuåsen","doi":"10.1080/23723556.2021.1910008","DOIUrl":"https://doi.org/10.1080/23723556.2021.1910008","url":null,"abstract":"<p><p>Conflicts between transcription and replication are a major source of replication stress. Our recent findings show that proper dephosphorylation of Serine 5 in the carboxy-terminal domain (CTD) of DNA-directed RNA polymerase II subunit RPB1 is needed to prevent such conflicts in human cells.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1910008"},"PeriodicalIF":2.1,"publicationDate":"2021-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1910008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010566","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
A new interaction between BRCA2 and DDX5 promotes the repair of DNA breaks at transcribed chromatin. BRCA2和DDX5之间的新相互作用促进了转录染色质上DNA断裂的修复。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-04-14 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1910474
Belen Gómez-González, Gaetana Sessa, Aura Carreira, Andrés Aguilera
{"title":"A new interaction between BRCA2 and DDX5 promotes the repair of DNA breaks at transcribed chromatin.","authors":"Belen Gómez-González,&nbsp;Gaetana Sessa,&nbsp;Aura Carreira,&nbsp;Andrés Aguilera","doi":"10.1080/23723556.2021.1910474","DOIUrl":"https://doi.org/10.1080/23723556.2021.1910474","url":null,"abstract":"<p><p>In a recent report, we have revealed a new interaction between the BRCA2 DNA repair associated protein (BRCA2) and the DEAD-box helicase 5 (DDX5) at DNA breaks that promotes unwinding DNA-RNA hybrids within transcribed chromatin and favors repair. Interestingly, BRCA2-DDX5 interaction is impaired in cells expressing the <i>BRCA2<sup>T2</sup> <sup>07A</sup></i> missense variant found in breast cancer patients.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1910474"},"PeriodicalIF":2.1,"publicationDate":"2021-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1910474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010568","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
EPHA2, a promising therapeutic target for hepatocellular carcinoma. EPHA2--肝细胞癌的有望治疗靶点。
IF 2.6
Molecular and Cellular Oncology Pub Date : 2021-04-14 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1910009
Hao Wang, Wei Qiu
{"title":"EPHA2, a promising therapeutic target for hepatocellular carcinoma.","authors":"Hao Wang, Wei Qiu","doi":"10.1080/23723556.2021.1910009","DOIUrl":"10.1080/23723556.2021.1910009","url":null,"abstract":"<p><p>Identifying critical drivers of oncogenesis and tumor progression is essential for developing effective hepatocellular carcinoma (HCC) therapeutics. Our recent findings has demonstrated that targeting Ephrin Receptor A2 (EPHA2) suppresses HCC initiation and progression by dual inhibition of the Protein Kinase B (AKT) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1910009"},"PeriodicalIF":2.6,"publicationDate":"2021-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128187/pdf/KMCO_8_1910009.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010567","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
Metabolic checkpoint of ferroptosis resistance. 铁下垂抵抗代谢检查点。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-31 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1901558
Jiao Liu, Rui Kang, Daolin Tang
{"title":"Metabolic checkpoint of ferroptosis resistance.","authors":"Jiao Liu,&nbsp;Rui Kang,&nbsp;Daolin Tang","doi":"10.1080/23723556.2021.1901558","DOIUrl":"https://doi.org/10.1080/23723556.2021.1901558","url":null,"abstract":"<p><p>The metabolic checkpoint of ferroptosis remains obscure. We find that glucose favors system xc<sup>-</sup> inhibitor-induced ferroptosis by activating pyruvate oxidation, thereby promoting fatty acid synthesis and subsequent lipid peroxidation. In contrast, the upregulation of pyruvate dehydrogenase kinase 4 (PDK4) switches into a ferroptosis-resistant state in pancreatic cancer cells.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1901558"},"PeriodicalIF":2.1,"publicationDate":"2021-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1901558","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010562","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: 6
The role of OFD1 in selective autophagy. OFD1在选择性自噬中的作用。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-31 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1903291
Brunella Franco, Manuela Morleo
{"title":"The role of OFD1 in selective autophagy.","authors":"Brunella Franco,&nbsp;Manuela Morleo","doi":"10.1080/23723556.2021.1903291","DOIUrl":"https://doi.org/10.1080/23723556.2021.1903291","url":null,"abstract":"<p><p>Autophagy is a cellular self-degradative pathway. Our study unveiled a novel mechanism mediated by OFD1, the protein mutated in Oral-Facial-Digital type I syndrome, based on selective degradation of autophagic proteins, which enables cells to calibrate their self-degradation. We demonstrated that unrestrained autophagy contributes to renal cysts observed in <i>Ofd1</i> mutants.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1903291"},"PeriodicalIF":2.1,"publicationDate":"2021-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1903291","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010564","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
The complex role of SIRT7 in p53 stabilization: nucleophosmin joins the debate. SIRT7在p53稳定中的复杂作用:核磷蛋白加入了争论。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-31 DOI: 10.1080/23723556.2021.1896349
Poonam Kumari, Shahriar Tarighi, Thomas Braun, Alessandro Ianni
{"title":"The complex role of SIRT7 in p53 stabilization: nucleophosmin joins the debate.","authors":"Poonam Kumari,&nbsp;Shahriar Tarighi,&nbsp;Thomas Braun,&nbsp;Alessandro Ianni","doi":"10.1080/23723556.2021.1896349","DOIUrl":"https://doi.org/10.1080/23723556.2021.1896349","url":null,"abstract":"<p><p>Release of nucleophosmin (NPM) from nucleoli following stress promotes rapid stabilization of the tumor suppressor p53 (TP53, best known as p53). Nucleoplasmic NPM binds to the ubiquitin ligase mouse double minute 2 (MDM2) and prevents MDM2-dependent p53 degradation. We recently demonstrated that sirtuin 7 (SIRT7) activates this pathway by directly deacetylating NPM following ultraviolet irradiation, indicating tumor-suppressive functions of SIRT7.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1896349"},"PeriodicalIF":2.1,"publicationDate":"2021-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1896349","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010560","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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