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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
The PIDDosome: centrosome guardian and backup on the DNA damage response. PIDDosome:中心体对DNA损伤反应的守护和备份。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-28 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1893625
Matteo Burigotto, Luca L Fava
{"title":"The PIDDosome: centrosome guardian and backup on the DNA damage response.","authors":"Matteo Burigotto,&nbsp;Luca L Fava","doi":"10.1080/23723556.2021.1893625","DOIUrl":"https://doi.org/10.1080/23723556.2021.1893625","url":null,"abstract":"<p><p>The PIDDosome is a Caspase-2-activating platform assembling in response to centrosome amplification or genotoxic stress. We have recently shown that both stimuli depend on ANKRD26 (ankyrin repeat domain-containing protein 26)-mediated localization of PIDD1 (p53-inducible protein with death domain) at the centrosome, demonstrating how this organelle can directly influence cell fate.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1893625"},"PeriodicalIF":2.1,"publicationDate":"2021-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1893625","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010558","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
Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma. 靶向单碳代谢需要mTOR抑制:骨肉瘤的新治疗方法
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-25 DOI: 10.1080/23723556.2021.1902250
Richa Rathore, Brian Van Tine
{"title":"Targeting one-carbon metabolism requires mTOR inhibition: a new therapeutic approach in osteosarcoma.","authors":"Richa Rathore,&nbsp;Brian Van Tine","doi":"10.1080/23723556.2021.1902250","DOIUrl":"https://doi.org/10.1080/23723556.2021.1902250","url":null,"abstract":"<p><p>The rate-limiting enzyme of serine biosynthesis, 3-phosphoglycerate dehydrogenase (PHGDH), contributes to rapid growth and proliferation when it is overexpressed in cancer. We recently described the metabolic adaptations that occur upon PHGDH inhibition in osteosarcoma. PHGDH inhibition causes metabolite accumulation that activates the mechanistic target of rapamycin (mTOR) signaling, sensitizing osteosarcoma to non-rapalog mTOR inhibition.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 3","pages":"1902250"},"PeriodicalIF":2.1,"publicationDate":"2021-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1902250","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010563","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
Phosphoglycerate mutase 1 (PGAM1) overexpression promotes radio- and chemoresistance in gliomas by activating the DNA damage response. 磷酸甘油酸突变酶1 (PGAM1)过表达通过激活DNA损伤反应促进胶质瘤的放射和化疗耐药。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-22 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1875804
Tor-Christian Aase Johannessen, Joydeep Mukherjee
{"title":"Phosphoglycerate mutase 1 (PGAM1) overexpression promotes radio- and chemoresistance in gliomas by activating the DNA damage response.","authors":"Tor-Christian Aase Johannessen,&nbsp;Joydeep Mukherjee","doi":"10.1080/23723556.2021.1875804","DOIUrl":"https://doi.org/10.1080/23723556.2021.1875804","url":null,"abstract":"<p><p>The glycolytic enzyme PGAM1 is overexpressed in gliomas where it efficiently facilitates the repair of DNA damage. Mechanistically, PGAM1 prevents inactivation of the ataxia-telangiectasia mutated (ATM) signaling pathway by sequestering the wild-type p53-induced phosphatase 1 (WIP1) in the cytoplasm. Genetic inhibition of PGAM1 expression subsequently sensitizes glioma cells against irradiation and chemotherapy-induced DNA damage.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1875804"},"PeriodicalIF":2.1,"publicationDate":"2021-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1875804","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38811570","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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