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CHMP4C: A novel regulator of the mitotic spindle checkpoint. CHMP4C:一种新的有丝分裂纺锤体检查点调节因子。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-11 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1445944
Eleni Petsalaki, George Zachos
{"title":"CHMP4C: A novel regulator of the mitotic spindle checkpoint.","authors":"Eleni Petsalaki,&nbsp;George Zachos","doi":"10.1080/23723556.2018.1445944","DOIUrl":"https://doi.org/10.1080/23723556.2018.1445944","url":null,"abstract":"<p><p>The mitotic spindle checkpoint delays anaphase onset until all chromosomes have achieved stable kinetochore-microtubule attachments. Here, we discuss recent findings showing that CHMP4C, a component of the endosomal sorting complex required for transport (ESCRT) machinery, protects human cells against chromosome missegregation by promoting localisation of the ROD-ZW10-ZWILCH (RZZ) spindle checkpoint complex to unattached kinetochores.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1445944"},"PeriodicalIF":2.1,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1445944","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519907","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: 7
Autophagy-independent effects of autophagy-related-5 (Atg5) on exosome production and metastasis. 自噬相关-5 (Atg5)对外泌体产生和转移的自噬非依赖性作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-11 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1445941
Huishan Guo, Remy Sadoul, Derrick Gibbings
{"title":"Autophagy-independent effects of autophagy-related-5 (Atg5) on exosome production and metastasis.","authors":"Huishan Guo,&nbsp;Remy Sadoul,&nbsp;Derrick Gibbings","doi":"10.1080/23723556.2018.1445941","DOIUrl":"https://doi.org/10.1080/23723556.2018.1445941","url":null,"abstract":"<p><p>Autophagy-related-5 (Atg5) and Autophagy-related-16-Like-1 (Atg16L1) canonically participate in autophagy. Recent research demonstrates that apart from this, they also control production of extracellular vesicles called exosomes by regulating acidification of late endosomes. Atg5-mediated exosome production increased migration and metastasis of breast cancer cells suggesting exosomes may perform some functions ascribed to autophagy.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1445941"},"PeriodicalIF":2.1,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1445941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519905","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: 12
Targeting kinases with precision. 精确定位激酶。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-11 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1435183
Alexandra K Gardino, Erica K Evans, Joseph L Kim, Natasja Brooijmans, Brian L Hodous, Beni Wolf, Christoph Lengauer
{"title":"Targeting kinases with precision.","authors":"Alexandra K Gardino,&nbsp;Erica K Evans,&nbsp;Joseph L Kim,&nbsp;Natasja Brooijmans,&nbsp;Brian L Hodous,&nbsp;Beni Wolf,&nbsp;Christoph Lengauer","doi":"10.1080/23723556.2018.1435183","DOIUrl":"https://doi.org/10.1080/23723556.2018.1435183","url":null,"abstract":"<p><p>Cancer genomics and mechanistic studies have revealed that heterogeneous mutations within a single kinase can result in a variety of activation mechanisms. The challenge has been to match these insights with tailored drug discovery strategies to yield potent, highly selective drugs. With optimized drugs in hand, physicians could apply the principles of personalized medicine with an increasing number of options to treat patients with improved precision according to their tumor's molecular genotype.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1435183"},"PeriodicalIF":2.1,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1435183","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521985","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
Asparagine, a critical limiting metabolite during glutamine starvation. 天冬酰胺，谷氨酰胺饥饿时的关键限制性代谢物。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-11 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1441633
Jie Jiang, Natalya N Pavlova, Ji Zhang
{"title":"Asparagine, a critical limiting metabolite during glutamine starvation.","authors":"Jie Jiang,&nbsp;Natalya N Pavlova,&nbsp;Ji Zhang","doi":"10.1080/23723556.2018.1441633","DOIUrl":"https://doi.org/10.1080/23723556.2018.1441633","url":null,"abstract":"<p><p>A challenge of targeting glutamine metabolism in cancer is that tumor cells develop various strategies to adapt to glutamine limitation. We found that asparagine plays a critical role in supporting protein synthesis during glutamine starvation, highlighting a possible approach to optimize the therapeutic efficacy of targeting glutamine metabolism in cancer.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1441633"},"PeriodicalIF":2.1,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1441633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519903","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: 16
LPCAT2 controls chemoresistance in colorectal cancer. LPCAT2控制结直肠癌的化疗耐药。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-11 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1448245
Alexia Karen Cotte, Virginie Aires, François Ghiringhelli, Dominique Delmas
{"title":"LPCAT2 controls chemoresistance in colorectal cancer.","authors":"Alexia Karen Cotte,&nbsp;Virginie Aires,&nbsp;François Ghiringhelli,&nbsp;Dominique Delmas","doi":"10.1080/23723556.2018.1448245","DOIUrl":"https://doi.org/10.1080/23723556.2018.1448245","url":null,"abstract":"<p><p>Lipid droplets (LD) are now-well recognized as playing a role in cancer progression, however their potential role in chemoresistance remains largely unknown, particularly in colorectal cancer (CRC). We recently highlighted that LD accumulate in CRC cells under the control of lysophosphatidylcholine acyltransferase 2 (LPCAT2) enzyme expression. We also showed that chemotherapy-induced LD accumulation counteracts intrinsic and extrinsic cancer cell death activation.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1448245"},"PeriodicalIF":2.1,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1448245","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519909","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
A new mechanism for LKB1 activation. LKB1激活的新机制。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-10 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2015.1035691
Szu-Wei Lee, Hui-Kuan Lin
{"title":"A new mechanism for LKB1 activation.","authors":"Szu-Wei Lee,&nbsp;Hui-Kuan Lin","doi":"10.1080/23723556.2015.1035691","DOIUrl":"https://doi.org/10.1080/23723556.2015.1035691","url":null,"abstract":"<p><p>Liver kinase B1 (LKB1, also known as serine/threonine kinase 11, STK11) has been thought to be a constitutively active tumor suppressor that is activated by forming an active complex. Very recently, a new post-translational modification on LKB1 was identified that can regulate LKB1 activation and LKB1-mediated cancer cell survival under energy stress.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1035691"},"PeriodicalIF":2.1,"publicationDate":"2018-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2015.1035691","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522040","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: 5
Linking SLAMF1 to autophagy and sensitivity to therapy in chronic lymphocytic leukemia. 慢性淋巴细胞白血病中SLAMF1与自噬和治疗敏感性的联系。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-10 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2016.1143077
Cinzia Bologna, Silvia Deaglio
{"title":"Linking SLAMF1 to autophagy and sensitivity to therapy in chronic lymphocytic leukemia.","authors":"Cinzia Bologna,&nbsp;Silvia Deaglio","doi":"10.1080/23723556.2016.1143077","DOIUrl":"https://doi.org/10.1080/23723556.2016.1143077","url":null,"abstract":"<p><p>We recently reported that expression of the costimulatory molecule and microbial sensor SLAMF1 (signaling lymphocytic activation molecule family 1, also known as CD150) is lost in chronic lymphocytic leukemia (CLL) patients characterized by a shorter overall survival. SLAMF1 modulates CLL responses to chemokines and regulates autophagy. Loss of SLAMF1 renders CLL cells relatively unresponsive to autophagy-inducing drugs, including B-cell CLL/lymphoma 2 (BCL2) inhibitors.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1143077"},"PeriodicalIF":2.1,"publicationDate":"2018-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2016.1143077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522043","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 histone variant macroH2A1 is a splicing-modulated caretaker of genome integrity and tumor growth. 组蛋白变体macroH2A1是剪接调节的基因组完整性和肿瘤生长的看护者。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-04 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1441629
Jeongkyu Kim, Philipp Oberdoerffer, Simran Khurana
{"title":"The histone variant macroH2A1 is a splicing-modulated caretaker of genome integrity and tumor growth.","authors":"Jeongkyu Kim,&nbsp;Philipp Oberdoerffer,&nbsp;Simran Khurana","doi":"10.1080/23723556.2018.1441629","DOIUrl":"https://doi.org/10.1080/23723556.2018.1441629","url":null,"abstract":"<p><p>The macroH2A1.2 histone variant facilitates the response to replication stress with implications for genome maintenance and cell growth. A mutually exclusive splice variant, macroH2A1.1, has opposing effects on DNA repair outcome and proliferation. Here we discuss the potential impact of splicing-modulated macroH2A1 chromatin organization for cell function and malignant transformation.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1441629"},"PeriodicalIF":2.1,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1441629","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519901","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: 13
Feedback regulation of mitochondrial homeostasis via Wnt/β-catenin signaling. 通过Wnt/β-catenin信号反馈调节线粒体稳态。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-04 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1458015
Dominic B Bernkopf, Jürgen Behrens
{"title":"Feedback regulation of mitochondrial homeostasis via Wnt/β-catenin signaling.","authors":"Dominic B Bernkopf,&nbsp;Jürgen Behrens","doi":"10.1080/23723556.2018.1458015","DOIUrl":"https://doi.org/10.1080/23723556.2018.1458015","url":null,"abstract":"<p><p>Cellular abundance of mitochondria is dynamically regulated. We could recently show that dysfunctional mitochondria release the phosphatase PGAM family member 5 (PGAM5) into the cytosol, where it interacts with the Wnt signaling-component AXIN1 and dephosphorylates AXIN1-bound β-catenin (CTNNB1) thereby activating Wnt/β-catenin signaling. Because Wnt/β-catenin signaling induces mitochondrial biogenesis dysfunctional mitochondria trigger their own replacement by releasing PGAM5.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1458015"},"PeriodicalIF":2.1,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1458015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519912","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
AMPK lifts the PRC2-implemented gene repression. AMPK解除prc2实施的基因抑制。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-04 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1441632
Tao Han, Qing Yin, Lixin Wan
{"title":"AMPK lifts the PRC2-implemented gene repression.","authors":"Tao Han,&nbsp;Qing Yin,&nbsp;Lixin Wan","doi":"10.1080/23723556.2018.1441632","DOIUrl":"https://doi.org/10.1080/23723556.2018.1441632","url":null,"abstract":"<p><p>The crosstalk between cellular energy status and epigenetic modifications remains largely elusive. We recently uncovered that upon energy restriction, AMP-activated protein kinase (AMPK) phosphorylates enhancer of zeste homolog 2 (EZH2), which disrupts the integrity of the polycomb repressive complex 2 (PRC2), thus inhibiting PRC2 oncogenic functions in ovarian and breast cancer cells.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1441632"},"PeriodicalIF":2.1,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1441632","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519902","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
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