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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
Cell-to-cell transmission of p53 aggregates: a novel player in oncology? p53聚集体的细胞间传递:肿瘤中的新角色?
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-22 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1892444
Naoyuki Iwahashi, Midori Ikezaki, Hiroyuki Saito, Kenji Uchimura, Kazuchika Nishitsuji
{"title":"Cell-to-cell transmission of p53 aggregates: a novel player in oncology?","authors":"Naoyuki Iwahashi,&nbsp;Midori Ikezaki,&nbsp;Hiroyuki Saito,&nbsp;Kenji Uchimura,&nbsp;Kazuchika Nishitsuji","doi":"10.1080/23723556.2021.1892444","DOIUrl":"https://doi.org/10.1080/23723556.2021.1892444","url":null,"abstract":"<p><p>The mutants of the tumor suppressor protein p53 form protein aggregates. It has been proposed that these aggregates propagate like prions, albeit the detailed mechanism of the propagation is unclear. Our recent study revealed that sulfated glycosaminoglycans, especially highly sulfated domains of heparan sulfate (heparan sulfate S-domains), participate in cancer pathology by mediating transcellular propagation of p53 aggregates.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1892444"},"PeriodicalIF":2.1,"publicationDate":"2021-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1892444","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38877807","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
p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control. p62/SQSTM1液滴启动自噬体生物发生和氧化应激控制。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-09 DOI: 10.1080/23723556.2021.1890990
Eeva-Liisa Eskelinen, Shun Kageyama, Masaaki Komatsu
{"title":"p62/SQSTM1 droplets initiate autophagosome biogenesis and oxidative stress control.","authors":"Eeva-Liisa Eskelinen,&nbsp;Shun Kageyama,&nbsp;Masaaki Komatsu","doi":"10.1080/23723556.2021.1890990","DOIUrl":"https://doi.org/10.1080/23723556.2021.1890990","url":null,"abstract":"<p><p>Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve as platforms for autophagosome formation and nuclear factor erythroid 2-related factor 2 (NRF2) activation. Further, p62-mediated NRF2 activation is not cytotoxic, but combination of NRF2 activation with impaired bulk and selective autophagy causes liver injury.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1890990"},"PeriodicalIF":2.1,"publicationDate":"2021-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1890990","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38875125","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
Control of S phase duration: a replication capacity model with E2F transcription at its heart. S 期持续时间的控制：以 E2F 转录为核心的复制能力模型
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-08 DOI: 10.1080/23723556.2020.1839294
Cosetta Bertoli, Robertus A M de Bruin
{"title":"Control of S phase duration: a replication capacity model with E2F transcription at its heart.","authors":"Cosetta Bertoli, Robertus A M de Bruin","doi":"10.1080/23723556.2020.1839294","DOIUrl":"10.1080/23723556.2020.1839294","url":null,"abstract":"<p><p>DNA replication capacity, the maximal amount of DNA a cell can synthesize at any given time during S phase, is controlled by E2F-dependent transcription. Controlling replication capacity limits the replication rate and provides a robust mechanism to keep replication fork speed within an optimal range whilst ensuring timely completion of genome duplication.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1839294"},"PeriodicalIF":2.1,"publicationDate":"2021-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0d/25/KMCO_8_1839294.PMC8018357.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38880246","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
Structure of Rad5 provides insights into its role in tolerance to replication stress. Rad5的结构提供了对其在耐受复制胁迫中的作用的见解。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-03-04 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1889348
Miaomiao Shen, Nalini Dhingra, Quan Wang, Xiaoxin Gong, Xin Xu, Hengyao Niu, Xiaolan Zhao, Song Xiang
{"title":"Structure of Rad5 provides insights into its role in tolerance to replication stress.","authors":"Miaomiao Shen,&nbsp;Nalini Dhingra,&nbsp;Quan Wang,&nbsp;Xiaoxin Gong,&nbsp;Xin Xu,&nbsp;Hengyao Niu,&nbsp;Xiaolan Zhao,&nbsp;Song Xiang","doi":"10.1080/23723556.2021.1889348","DOIUrl":"https://doi.org/10.1080/23723556.2021.1889348","url":null,"abstract":"<p><p>The Rad5 family of proteins are critical genome maintenance factors, with helicase-like transcription factor (HLTF) and SNF2 histone linker PHD RING helicase (SHRPH) in humans implicated in several types of cancer. How their multiple activities coordinate has been unclear. Our recent study on Rad5 shed light on this question.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1889348"},"PeriodicalIF":2.1,"publicationDate":"2021-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1889348","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38877806","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
Trex2 responds to damaged replication forks in diverse ways. Trex2以不同的方式对受损的复制分叉做出反应。
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-02-25 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1881394
Paul Hasty
{"title":"Trex2 responds to damaged replication forks in diverse ways.","authors":"Paul Hasty","doi":"10.1080/23723556.2021.1881394","DOIUrl":"https://doi.org/10.1080/23723556.2021.1881394","url":null,"abstract":"<p><p>Three prime Repair Exonuclease 2 (Trex2) alters replication fork (RF) stability and mutation levels in cells defective for homologous recombination (HR). Trex2 has multiple functions that can either cause or supress RF instability in cells with different HR-defects. Why does Trex2 have such diverse effects on RF maintenance?</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1881394"},"PeriodicalIF":2.1,"publicationDate":"2021-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1881394","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38877803","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
Tuning protein synthesis for cancer therapy. 调控蛋白质合成以治疗癌症
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-02-22 DOI: 10.1080/23723556.2021.1884034
John R P Knight, Owen J Sansom
{"title":"Tuning protein synthesis for cancer therapy.","authors":"John R P Knight, Owen J Sansom","doi":"10.1080/23723556.2021.1884034","DOIUrl":"10.1080/23723556.2021.1884034","url":null,"abstract":"<p><p>~50% of colorectal cancers have an activating mutation in <i>KRAS</i> (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevated c-MYC (MYC proto-oncogene) expression. Targeting these pathways downstream of KRAS reveals a striking dependency that has potential for clinical translation.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1884034"},"PeriodicalIF":2.1,"publicationDate":"2021-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38875124","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
MaTAR25: a long non-coding RNA involved in breast cancer progression. MaTAR25:参与乳腺癌进展的长链非编码RNA
IF 2.1
Molecular and Cellular Oncology Pub Date : 2021-02-22 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1882286
Kung-Chi Chang, David L Spector
{"title":"<i>MaTAR25</i>: a long non-coding RNA involved in breast cancer progression.","authors":"Kung-Chi Chang,&nbsp;David L Spector","doi":"10.1080/23723556.2021.1882286","DOIUrl":"https://doi.org/10.1080/23723556.2021.1882286","url":null,"abstract":"<p><p>We recently reported on the role of <i>Mammary Tumor Associated RNA 25</i> (<i>MaTAR25</i>) in mammary tumor cell proliferation, migration, and invasion. <i>MaTAR25</i> interacts with transcriptional activator protein Pur-beta (Purb) to regulate its downstream targets such as <i>Tensin1</i> in <i>trans</i>. The human ortholog of <i>MaTAR25, LINC01271</i>, is upregulated with human breast cancer stage and metastasis.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 2","pages":"1882286"},"PeriodicalIF":2.1,"publicationDate":"2021-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2021.1882286","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38877805","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
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