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Loss of histone acetylation and H3K4 methylation promotes melanocytic malignant transformation. 组蛋白乙酰化和H3K4甲基化的缺失促进黑素细胞恶性转化。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-02-26 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1359229
Ayush T Raman, Kunal Rai
{"title":"Loss of histone acetylation and H3K4 methylation promotes melanocytic malignant transformation.","authors":"Ayush T Raman,&nbsp;Kunal Rai","doi":"10.1080/23723556.2017.1359229","DOIUrl":"https://doi.org/10.1080/23723556.2017.1359229","url":null,"abstract":"<p><p>Epigenetic mechanisms play essential roles in biological processes such as cell maintenance, differentiation, proliferation and apoptosis. A recent report from our laboratory showed that the loss of histone acetylation and H3K4 (Histone H3 Lysine 4) methylation in the proximal regions of cancer regulatory genes promote tumorigenesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1359229"},"PeriodicalIF":2.1,"publicationDate":"2018-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1359229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521979","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
An unexpected tumor suppressor role for VAV1a. VAV1a的意想不到的肿瘤抑制作用。
Molecular & cellular oncology Pub Date : 2018-02-23 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1432257
Xosé R Bustelo, L Francisco Lorenzo-Martín, Myriam Cuadrado, Isabel Fernández-Pisonero, Javier Robles-Valero
{"title":"An unexpected tumor suppressor role for VAV1<sup>a</sup>.","authors":"Xosé R Bustelo, L Francisco Lorenzo-Martín, Myriam Cuadrado, Isabel Fernández-Pisonero, Javier Robles-Valero","doi":"10.1080/23723556.2018.1432257","DOIUrl":"10.1080/23723556.2018.1432257","url":null,"abstract":"<p><p>RHO GDP/GTP exchange factors, including VAV1, are considered key protumorigenic factors. Against this paradigm, we have found that VAV1 plays tumor suppressor roles by buffering NOTCH1 signals in thymocytes. The silencing of this pathway contributes to the pathogenesis of T cell acute lymphoblastic leukemia of the early cortical, TLX<sup>+</sup> subtype.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1432257"},"PeriodicalIF":0.0,"publicationDate":"2018-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6149884/pdf/kmco-05-03-1432257.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521982","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
Senescence drives non-cell autonomous tumorigenesis in the pituitary gland. 衰老驱动垂体非细胞自主肿瘤发生。
Molecular & cellular oncology Pub Date : 2018-02-13 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1435180
Jose Mario Gonzalez-Meljem, Juan Pedro Martinez-Barbera
{"title":"Senescence drives non-cell autonomous tumorigenesis in the pituitary gland.","authors":"Jose Mario Gonzalez-Meljem, Juan Pedro Martinez-Barbera","doi":"10.1080/23723556.2018.1435180","DOIUrl":"10.1080/23723556.2018.1435180","url":null,"abstract":"<p><p>Novel detrimental functions of senescent cells have been recently uncovered in the context of cancer development and progression, which they mainly exert through the secretion of several pro-tumorigenic factors. Here we discuss how cellular senescence and its secretory phenotype can be involved in the widely unexplored phenomenon of paracrine tumorigenesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1435180"},"PeriodicalIF":0.0,"publicationDate":"2018-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/13/bc/kmco-05-03-1435180.PMC5964449.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36200337","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
Crosstalk between p53 modifiers at PML bodies. PML小体p53修饰子间的串扰。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-02-08 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2015.1074335
Sonja Matt, Thomas G Hofmann
{"title":"Crosstalk between p53 modifiers at PML bodies.","authors":"Sonja Matt,&nbsp;Thomas G Hofmann","doi":"10.1080/23723556.2015.1074335","DOIUrl":"https://doi.org/10.1080/23723556.2015.1074335","url":null,"abstract":"<p><p>Tumor protein p53 (TP53, best known as p53), the most frequently mutated tumor suppressor in cancer, plays a central role in cell fate decisions induced by DNA damage. Regulation of p53 activity by post-translational modifications has been linked to promyelocytic leukemia nuclear bodies (PML-NBs), where p53 encounters many of its regulators. Recent evidence implies that crosstalk between p53 regulators at the PML-NB shapes post-translational modifications and function of p53.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1074335"},"PeriodicalIF":2.1,"publicationDate":"2018-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2015.1074335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522042","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: 11
ARF-NRF2: A new checkpoint for oxidative stress responses? ARF-NRF2:氧化应激反应的新检查点?
IF 2.1
Molecular & cellular oncology Pub Date : 2018-02-06 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1432256
Delin Chen, Omid Tavana, Wei Gu
{"title":"ARF-NRF2: A new checkpoint for oxidative stress responses?","authors":"Delin Chen,&nbsp;Omid Tavana,&nbsp;Wei Gu","doi":"10.1080/23723556.2018.1432256","DOIUrl":"https://doi.org/10.1080/23723556.2018.1432256","url":null,"abstract":"<p><p>NRF2 (nuclear factor erythroid 2-related factor 2) is a transcription factor which plays a major role in oxidative stress responses by regulating antioxidant gene expression. We have recently identified the ARF tumor suppressor as a key regulator of NRF2. ARF can significantly inhibit NRF2 transcriptional activities, and the ARF-NRF2 interaction may function as a novel checkpoint for oxidative stress responses.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1432256"},"PeriodicalIF":2.1,"publicationDate":"2018-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1432256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521981","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: 9
Escaping NK cells and recruiting neutrophils: How Morgana/NF-κB signaling promotes metastasis. 逃逸NK细胞和募集中性粒细胞:Morgana/NF-κB信号如何促进转移。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-01-30 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1432258
Federica Fusella, Laura Seclì, Mara Brancaccio
{"title":"Escaping NK cells and recruiting neutrophils: How Morgana/NF-κB signaling promotes metastasis.","authors":"Federica Fusella,&nbsp;Laura Seclì,&nbsp;Mara Brancaccio","doi":"10.1080/23723556.2018.1432258","DOIUrl":"https://doi.org/10.1080/23723556.2018.1432258","url":null,"abstract":"<p><p>Cancer cells escape immune surveillance and induce immune cell aberrant activation to support tumour growth and progression. We recently reported that Morgana/NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling in breast cancer cells is responsible for NK (Natural Killer) cell inactivation and neutrophil recruitment in the primary tumour and in the lung pre-metastatic niche.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1432258"},"PeriodicalIF":2.1,"publicationDate":"2018-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1432258","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521983","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
Aggressive leukemia driven by MLL-AF9. MLL-AF9驱动的侵袭性白血病。
IF 2.1
Molecular & cellular oncology Pub Date : 2017-10-23 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2016.1241854
Vaia Stavropoulou, Antoine H F M Peters, Juerg Schwaller
{"title":"Aggressive leukemia driven by MLL-AF9.","authors":"Vaia Stavropoulou,&nbsp;Antoine H F M Peters,&nbsp;Juerg Schwaller","doi":"10.1080/23723556.2016.1241854","DOIUrl":"https://doi.org/10.1080/23723556.2016.1241854","url":null,"abstract":"<p><p>We recently showed that cellular origin impacts the aggressiveness and the phenotype of acute myeloid leukemia (AML). Direct induction of the MLL-AF9 fusion in various hematopoietic compartments <i>in vivo</i> using a doxycycline (DOX) regulated mouse model (iMLL-AF9) led to an invasive chemoresistant AML expressing several genes known to be involved in epithelial to mesenchymal transition (EMT) in solid cancers. Many of these genes play important roles in migration and invasion and are significantly associated with poor overall survival in AML patients.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1241854"},"PeriodicalIF":2.1,"publicationDate":"2017-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2016.1241854","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522046","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: 10
Dual targeting of EGFR and glutaminase in lung cancer. EGFR和谷氨酰胺酶在肺癌中的双重靶向作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2017-04-19 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1297883
Milica Momcilovic, David B Shackelford
{"title":"Dual targeting of EGFR and glutaminase in lung cancer.","authors":"Milica Momcilovic,&nbsp;David B Shackelford","doi":"10.1080/23723556.2017.1297883","DOIUrl":"https://doi.org/10.1080/23723556.2017.1297883","url":null,"abstract":"<p><p>We have recently demonstrated that targeted inhibition of epidermal growth factor receptor (EGFR) signaling and glutaminase led to metabolic crisis in <i>EGFR</i> mutant lung adenocarcinomas and significant tumor regression in mouse xenograft models. Combining targeted therapies that restrict the metabolic activity and growth of tumors represents a therapeutic strategy that holds promise for clinical translation.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1297883"},"PeriodicalIF":2.1,"publicationDate":"2017-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1297883","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521975","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
Nutrient availability dictates the regulation of metabolism by the ribosomal protein-MDM2-p53 pathway. 营养可利用性决定了核糖体蛋白- mdm2 -p53途径对代谢的调节。
IF 2.1
Molecular & cellular oncology Pub Date : 2017-04-03 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1302904
Derek Franklin, Yanping Zhang
{"title":"Nutrient availability dictates the regulation of metabolism by the ribosomal protein-MDM2-p53 pathway.","authors":"Derek Franklin,&nbsp;Yanping Zhang","doi":"10.1080/23723556.2017.1302904","DOIUrl":"https://doi.org/10.1080/23723556.2017.1302904","url":null,"abstract":"<p><p>Nutrient availability alters ribosomal biogenesis, causing ribosomal proteins to act as secondary messengers of nutrient response by binding to MDM2 and activating p53. Recent work suggests that the ribosomal protein (RP)-MDM2-p53 pathway responds to the deficiency or overabundance of nutrients through seemingly contradictory mechanisms; however, both of these responses promote organism survival.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1302904"},"PeriodicalIF":2.1,"publicationDate":"2017-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1302904","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521976","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
The roles of NANOG in tumorigenesis. NANOG在肿瘤发生中的作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2015-07-29 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2015.1074334
Jinchul Kim, Stefan Yu, Yang Xu
{"title":"The roles of NANOG in tumorigenesis.","authors":"Jinchul Kim,&nbsp;Stefan Yu,&nbsp;Yang Xu","doi":"10.1080/23723556.2015.1074334","DOIUrl":"https://doi.org/10.1080/23723556.2015.1074334","url":null,"abstract":"<p><p>The pluripotency factor Nanog is highly expressed in pluripotent stem cells and certain adult stem cells, but is not expressed in normal adult cells. However, Nanog is frequently overexpressed in human cancers. Here, we discuss the distinct oncogenic roles of Nanog at various stages of tumorigenesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1074334"},"PeriodicalIF":2.1,"publicationDate":"2015-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2015.1074334","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522041","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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