Haider M Hassan, Majdina Isovic, Michael Tully Underhill, Joseph Torchia
{"title":"TDG is a novel tumor suppressor of liver malignancies.","authors":"Haider M Hassan, Majdina Isovic, Michael Tully Underhill, Joseph Torchia","doi":"10.1080/23723556.2020.1768819","DOIUrl":"https://doi.org/10.1080/23723556.2020.1768819","url":null,"abstract":"<p><p>In a recent publication, we demonstrated that conditional deletion of the gene encoding thymine DNA glycosylase (TDG) leads to a late onset of hepatocellular carcinoma (HCC). TDG loss causes disruption in active DNA demethylation in the liver and dysregulation of the farnesoid X receptor and small heterodimer partner (FXR-SHP) regulatory cascade. This leads to a loss of bile acid and glucose homeostasis, which predisposes mice to HCC.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1768819"},"PeriodicalIF":2.1,"publicationDate":"2020-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1768819","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490011","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}
{"title":"Targeting CARM1 in ovarian cancer with EZH2 and PARP inhibitors.","authors":"Sergey Karakashev, Rugang Zhang","doi":"10.1080/23723556.2020.1760675","DOIUrl":"https://doi.org/10.1080/23723556.2020.1760675","url":null,"abstract":"<p><p>Coactivator-associated arginine methyltransferase 1 (<i>CARM1</i>)-expressing high-grade serous ovarian cancers are characterized by poor prognosis and limited therapeutic options. Here we discuss a novel therapeutic strategy to target CARM1-expressing ovarian cancer based on a combination of poly (ADP-ribose) polymerase (PARP) and enhancer of zeste homology 2 (EZH2) inhibitors.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1760675"},"PeriodicalIF":2.1,"publicationDate":"2020-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1760675","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490006","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}
{"title":"Targeting neurolysin in acute myeloid leukemia.","authors":"Sara Mirali, Aaron D Schimmer","doi":"10.1080/23723556.2020.1761243","DOIUrl":"https://doi.org/10.1080/23723556.2020.1761243","url":null,"abstract":"<p><p>We recently identified the mitochondrial peptidase, neurolysin (NLN), as a top hit in an acute myeloid leukemia (AML) viability screen. Using chemical and genetic approaches, we demonstrated that loss of NLN disrupted respiratory chain supercomplex assembly and impaired oxidative metabolism in AML. Moreover, inhibition of NLN <i>in vitro</i> and <i>in vivo</i> reduced the growth of AML cells.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1761243"},"PeriodicalIF":2.1,"publicationDate":"2020-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1761243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490008","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}
{"title":"Energy stress inhibits ferroptosis via AMPK.","authors":"Hyemin Lee, Li Zhuang, Boyi Gan","doi":"10.1080/23723556.2020.1761242","DOIUrl":"https://doi.org/10.1080/23723556.2020.1761242","url":null,"abstract":"<p><p>Energy stress disturbs cellular homeostasis and induces cell death. Our recent study revealed that ferroptosis (a non-apoptotic cell death) is an energy-requiring process, and energy stress-mediated activation of adenosine monophosphate-activated protein kinase (AMPK) inhibits ferroptosis. Mechanistically, AMPK regulates ferroptosis through acetyl-CoA carboxylase (ACC) and polyunsaturated fatty acid (PUFA) biosynthesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1761242"},"PeriodicalIF":2.1,"publicationDate":"2020-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1761242","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490007","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}
{"title":"Unbiased translation proteomics upon cell stress.","authors":"Kevin Klann, Christian Münch","doi":"10.1080/23723556.2020.1763150","DOIUrl":"https://doi.org/10.1080/23723556.2020.1763150","url":null,"abstract":"<p><p>The mammalian target of rapamycin and the integrated stress response are central cellular hubs regulating translation upon stress. The precise proteins and pathway specificity of translation targets of these pathways remained largely unclear. We recently described a new method for quantitative translation proteomics and found that both pathways control translation of the same sets of proteins.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1763150"},"PeriodicalIF":2.1,"publicationDate":"2020-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1763150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490009","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}
{"title":"NORRIN plays a context-dependent role in glioblastoma stem cells.","authors":"Ahmed El-Sehemy, Valerie A Wallace","doi":"10.1080/23723556.2020.1758540","DOIUrl":"https://doi.org/10.1080/23723556.2020.1758540","url":null,"abstract":"<p><p>We recently reported a novel role of the atypical Wnt ligand, NORRIN, in mediating the proliferation and stemness of glioblastoma stem cells. Mechanistic and functional analysis revealed context-specific phenotypes in which NORRIN can induce opposite effects on the tumor outcome, depending on the underlying molecular signature of the tumor cells.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1758540"},"PeriodicalIF":2.1,"publicationDate":"2020-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1758540","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490004","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}
{"title":"LATS1-Beclin1 mediates a non-canonical connection between the Hippo pathway and autophagy.","authors":"Fengyuan Tang, Gerhard Christofori","doi":"10.1080/23723556.2020.1757378","DOIUrl":"https://doi.org/10.1080/23723556.2020.1757378","url":null,"abstract":"<p><p>Understanding the mechanisms of evasive resistance in cancer is of great importance to develop efficient therapies. Analyzing the molecular mechanisms underlying therapy resistance of hepatocellular carcinoma (HCC), we have discovered a kinase-activity independent role of LATS1 (large tumor suppressor) but not LATS2 in regulating sorafenib-induced lethal autophagy in HCC. We have found that the autophagy regulatory role of LATS1 is a general phenomenon in response to various stimuli of autophagy induction which relies on a LATS1-specific protein domain. Mechanistically, the autophagy regulatory role of LATS1 is coupled with Beclin-1 (BECN1) K27-linked ubiquitination and BECN1 self-dimerization. Our study highlights a LATS1-mediated non-classical interaction between the Hippo signaling pathway and autophagy in therapy response and carcinogenesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1757378"},"PeriodicalIF":2.1,"publicationDate":"2020-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1757378","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490003","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}
{"title":"Targeting tumor vulnerabilities associated with loss of heterozygosity.","authors":"Veronica Rendo, Ivaylo Stoimenov, Tobias Sjöblom","doi":"10.1080/23723556.2020.1759390","DOIUrl":"https://doi.org/10.1080/23723556.2020.1759390","url":null,"abstract":"<p><p>We show that N-acetyltransferase 2 (<i>NAT2</i>) loss of heterozygosity can be targeted in >4% of colorectal cancers with the use of a small molecule. We identify and describe the effect of a compound that impairs the growth of colorectal tumors with slow NAT2 activity by half when compared to wild-type.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1759390"},"PeriodicalIF":2.1,"publicationDate":"2020-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1759390","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490005","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}
Deborah A Silverman, George A Calin, Jeffrey N Myers, Moran Amit
{"title":"Neural reprogramming via microRNAs: the new kid on the p53-deficient block.","authors":"Deborah A Silverman, George A Calin, Jeffrey N Myers, Moran Amit","doi":"10.1080/23723556.2020.1756723","DOIUrl":"https://doi.org/10.1080/23723556.2020.1756723","url":null,"abstract":"<p><p>We recently reported a novel role for nerve-cancer crosstalk, demonstrating that tumor protein p53 (<i>TP53</i>) deficiency in head and neck squamous cell carcinoma leads to a decrease in miR-34a in tumor-shed vesicles. This directed sensory nerve reprogramming in the tumor microenvironment which enhanced tumor growth.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1756723"},"PeriodicalIF":2.1,"publicationDate":"2020-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1756723","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38490002","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}
{"title":"The plot thickens: OTULIN regulation in cell death.","authors":"Todd Douglas, Maya Saleh","doi":"10.1080/23723556.2020.1740541","DOIUrl":"https://doi.org/10.1080/23723556.2020.1740541","url":null,"abstract":"<p><p>We recently demonstrated that post-translational modifications of the OTU deubiquitinase with linear linkage specificity (OTULIN) regulate its function in cell death. OTULIN hyper-phosphorylation promotes necroptosis by locking ring finger protein 31 (RNF31, also known as HOIP) away from the cylindromatosis (CYLD) complex, resulting in altered receptor interacting serine/threonine kinase 1 (RIPK1) ubiquitination. Further, we identified dual specificity phosphatase 14 (DUSP14) as an OTULIN phosphatase that limits necroptosis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1740541"},"PeriodicalIF":2.1,"publicationDate":"2020-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1740541","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38392168","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}