Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2009423
Caiyun Liu, Xinjian Li
ABSTRACT How cancer cells absorb enough glucose to support their rapid growth is poorly understood. We have recently demonstrated that palmitoyl transferase DHHC9 palmitoylates glucose transporter GLUT1 at Cys207 to maintain GLUT1 plasma membrane localization. DHHC9-mediated GLUT1 palmitoylation supports glycolysis, proliferation, colony formation, and tumorigenicity of glioblastoma cells.
{"title":"Greasy GLUT1 maintains glioblastoma malignancy","authors":"Caiyun Liu, Xinjian Li","doi":"10.1080/23723556.2021.2009423","DOIUrl":"https://doi.org/10.1080/23723556.2021.2009423","url":null,"abstract":"ABSTRACT How cancer cells absorb enough glucose to support their rapid growth is poorly understood. We have recently demonstrated that palmitoyl transferase DHHC9 palmitoylates glucose transporter GLUT1 at Cys207 to maintain GLUT1 plasma membrane localization. DHHC9-mediated GLUT1 palmitoylation supports glycolysis, proliferation, colony formation, and tumorigenicity of glioblastoma cells.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42374549","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.1985930
Romain Villot, Audrey Poirier, R. Devillers, A. Kolnoguz, S. Elowe, V. Manem, P. Joubert, Frédérick A. Mallette, M. Laplante
ABSTRACT We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work.
{"title":"ZNF768: controlling cellular senescence and proliferation with ten fingers","authors":"Romain Villot, Audrey Poirier, R. Devillers, A. Kolnoguz, S. Elowe, V. Manem, P. Joubert, Frédérick A. Mallette, M. Laplante","doi":"10.1080/23723556.2021.1985930","DOIUrl":"https://doi.org/10.1080/23723556.2021.1985930","url":null,"abstract":"ABSTRACT We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46161742","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2010512
Mariana Paes Dias, J. Jonkers
ABSTRACT Tumors with loss of breast cancer type 1 susceptibility protein (BRCA1) are homologous recombination (HR) deficient and hypersensitive to poly(ADP-ribose) polymerase inhibitors (PARPi). However, these tumors may restore HR and acquire PARPi resistance via loss of end-protection of DNA double-strand breaks. We found that loss of nuclear DNA ligase III resensitizes HR-restored BRCA1-deficient cells to PARPi by exposing post-replicative single-stranded DNA (ssDNA) gaps. Our work, and that of others, identifies ssDNA gaps as a key determinant of PARPi response.
{"title":"Filling in the gaps in PARP inhibitor-induced synthetic lethality","authors":"Mariana Paes Dias, J. Jonkers","doi":"10.1080/23723556.2021.2010512","DOIUrl":"https://doi.org/10.1080/23723556.2021.2010512","url":null,"abstract":"ABSTRACT Tumors with loss of breast cancer type 1 susceptibility protein (BRCA1) are homologous recombination (HR) deficient and hypersensitive to poly(ADP-ribose) polymerase inhibitors (PARPi). However, these tumors may restore HR and acquire PARPi resistance via loss of end-protection of DNA double-strand breaks. We found that loss of nuclear DNA ligase III resensitizes HR-restored BRCA1-deficient cells to PARPi by exposing post-replicative single-stranded DNA (ssDNA) gaps. Our work, and that of others, identifies ssDNA gaps as a key determinant of PARPi response.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46061335","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2013723
Mariana Cooke
ABSTRACT In a recent study, our group identified RAC guanine nucleotide exchange factors (RAC-GEFs) driving motility signaling in KRAS mutant lung adenocarcinoma cells. The RAC-GEFs FARP1, ARHGEF39 and TIAM2 play fundamental roles in the formation of membrane ruffles in response to growth factor receptor stimulation.
{"title":"Novel insights into the RTK-dependent metastatic phenotype of KRAS-mutant lung adenocarcinoma","authors":"Mariana Cooke","doi":"10.1080/23723556.2021.2013723","DOIUrl":"https://doi.org/10.1080/23723556.2021.2013723","url":null,"abstract":"ABSTRACT In a recent study, our group identified RAC guanine nucleotide exchange factors (RAC-GEFs) driving motility signaling in KRAS mutant lung adenocarcinoma cells. The RAC-GEFs FARP1, ARHGEF39 and TIAM2 play fundamental roles in the formation of membrane ruffles in response to growth factor receptor stimulation.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49485087","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2009424
Bastian Stark, G. Poon, John J. Wyrick
ABSTRACT Somatic mutations in skin cancers are highly enriched at binding sites for CCCTC-binding factor (CTCF). We have discovered that CTCF binding alters the DNA structure to render it more susceptible to UV damage. Elevated UV damage formation at CTCF binding sites, in conjunction with subsequent repair inhibition, promotes UV mutagenesis.
{"title":"CTCF puts a new twist on UV damage and repair in skin cancer","authors":"Bastian Stark, G. Poon, John J. Wyrick","doi":"10.1080/23723556.2021.2009424","DOIUrl":"https://doi.org/10.1080/23723556.2021.2009424","url":null,"abstract":"ABSTRACT Somatic mutations in skin cancers are highly enriched at binding sites for CCCTC-binding factor (CTCF). We have discovered that CTCF binding alters the DNA structure to render it more susceptible to UV damage. Elevated UV damage formation at CTCF binding sites, in conjunction with subsequent repair inhibition, promotes UV mutagenesis.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42018351","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.1996318
Kazuhiro Fukumura, J. Venables, A. Mayeda
ABSTRACT The early splicing complex A occupies at least eighty nucleotides of intron, in which U2AF covers the polypyrimidine tract. SPF45 (RBM17) functionally substitutes for U2AF on a subset of short introns. Since SPF45 expression confers resistance to various anticancer drugs, SPF45-dependent splicing may play a critical role in multidrug resistance.
{"title":"SPF45/RBM17-dependent splicing and multidrug resistance to cancer chemotherapy","authors":"Kazuhiro Fukumura, J. Venables, A. Mayeda","doi":"10.1080/23723556.2021.1996318","DOIUrl":"https://doi.org/10.1080/23723556.2021.1996318","url":null,"abstract":"ABSTRACT The early splicing complex A occupies at least eighty nucleotides of intron, in which U2AF covers the polypyrimidine tract. SPF45 (RBM17) functionally substitutes for U2AF on a subset of short introns. Since SPF45 expression confers resistance to various anticancer drugs, SPF45-dependent splicing may play a critical role in multidrug resistance.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43957415","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2007030
A. García-García, I. Martin
ABSTRACT We propose an in vitro 3D culture system combining perfusion bioreactors, scaffolds and human primary cells to engineer fully-humanized, biomimetic and customizable bone marrow tissues. This system could serve as a model to investigate human hematopoietic stem cell niches, but also as a drug testing platform for pharmaceutical research and patient-personalized medicine.
{"title":"Biomimetic human bone marrow tissues: models to study hematopoiesis and platforms for drug testing","authors":"A. García-García, I. Martin","doi":"10.1080/23723556.2021.2007030","DOIUrl":"https://doi.org/10.1080/23723556.2021.2007030","url":null,"abstract":"ABSTRACT We propose an in vitro 3D culture system combining perfusion bioreactors, scaffolds and human primary cells to engineer fully-humanized, biomimetic and customizable bone marrow tissues. This system could serve as a model to investigate human hematopoietic stem cell niches, but also as a drug testing platform for pharmaceutical research and patient-personalized medicine.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49355986","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2007029
M. Llorens-Agost, M. Ensminger, H. Le, W. Heyer, M. Löbrich
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.
{"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":null,"pages":null},"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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.2011564
A. Bufe, S. Acebrón
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).
{"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":null,"pages":null},"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}
Pub Date : 2021-11-01eCollection Date: 2021-01-01DOI: 10.1080/23723556.2021.1984827
Navya Murugesan, Mayinuer Maitituoheti
We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-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.
{"title":"<i>KMT2D</i> deficiency confers a therapeutic vulnerability to glycolytic and <i>IGFR</i> inhibitors in melanoma.","authors":"Navya Murugesan, 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":null,"pages":null},"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}
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