{"title":"Eat this, not that! How selective autophagy helps cancer cells survive.","authors":"Robin Mathew, Eileen White","doi":"10.4161/23723556.2014.975638","DOIUrl":"https://doi.org/10.4161/23723556.2014.975638","url":null,"abstract":"<p><p>Autophagy degrades the cellular proteome to promote survival, but the underlying mechanism and substrates of consequence are poorly understood. We found that autophagy selectively remodels the proteome in cancer cells by eliminating proinflammatory signaling proteins. Autophagy ablation causes aberrant accumulation of these proteins that primes cancer cells for interferon-dependent cell death, explaining how autophagy suppresses inflammation and promotes tumor maintenance. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975638"},"PeriodicalIF":2.1,"publicationDate":"2015-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484596","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 control of tumor vessels: what you would not expect from a neural adhesion molecule.","authors":"Francesca Angiolini, Ugo Cavallaro","doi":"10.4161/23723556.2014.982045","DOIUrl":"10.4161/23723556.2014.982045","url":null,"abstract":"<p><p>The neural adhesion molecule L1 is involved in development and plasticity of the nervous system. We recently reported aberrant expression of L1 in the vasculature of various human tumor types. Genetic and functional inactivation of endothelial L1 in a mouse tumor model resulted in decreased tumor angiogenesis and promoted vascular normalization. Thus, endothelial L1 might represent a novel therapeutic target for vessel-targeted treatments of solid tumors. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e982045"},"PeriodicalIF":0.0,"publicationDate":"2015-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/35/7b/kmco-02-02-982045.PMC4904897.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34647767","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}
Adriana Soler, Ana Angulo-Urarte, Mariona Graupera
{"title":"PI3K at the crossroads of tumor angiogenesis signaling pathways.","authors":"Adriana Soler, Ana Angulo-Urarte, Mariona Graupera","doi":"10.4161/23723556.2014.975624","DOIUrl":"https://doi.org/10.4161/23723556.2014.975624","url":null,"abstract":"<p><p>Tumors need blood vessels for their growth, thus providing the rationale for antiangiogenic therapy in cancer treatment. However, intrinsic and acquired resistance and low response rates have turned out to be major limitations of antiangiogenic therapy. This emphasizes the need to further understand how the vasculature in cancer can be targeted. Although endothelial cells (ECs) rely on multiple growth factors and cytokines to grow, antiangiogenic therapies have mainly centered on targeting vascular endothelial growth factor (VEGF). Phosphoinositide 3-kinases (PI3Ks) form a family of 8 isoenzymes with non-redundant functions in normal biology and cancer. The subgroup of class I PI3Ks are situated at the crossroad of a plethora of proangiogenic signals and control cell growth, survival, motility, and metabolism. These isoenzymes have pleiotropic roles in the tumor microenvironment, including cell-autonomous functions in ECs, underscoring the complexity of targeting this pathway in cancer. Here, we describe how the PI3K axis influences angiogenesis in different cell compartments and summarize the diversity of vascular responses to PI3K inhibition. Targeting PI3K signaling by isoform-selective inhibitors, together with readjusting the current doses below the maximum tolerated dose, may improve clinical responses to class I PI3K anticancer agents. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975624"},"PeriodicalIF":2.1,"publicationDate":"2015-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975624","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484593","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":"PTP1B: mediating ROS signaling to silence genes.","authors":"Benoit Boivin, Nicholas K Tonks","doi":"10.4161/23723556.2014.975633","DOIUrl":"https://doi.org/10.4161/23723556.2014.975633","url":null,"abstract":"<p><p>Numerous studies have shown that normal cells often respond to the activation of oncogenes by undergoing reactive oxygen species-dependent induction of senescence. Here, we discuss our recent publication identifying protein tyrosine phosphatase PTP1B as an important redox-controlled checkpoint for senescence downstream of oncogenic RAS. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975633"},"PeriodicalIF":2.1,"publicationDate":"2015-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484594","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":"Oncogenic long noncoding RNA FAL1 in human cancer.","authors":"Xiaomin Zhong, Xiaowen Hu, Lin Zhang","doi":"10.4161/23723556.2014.977154","DOIUrl":"https://doi.org/10.4161/23723556.2014.977154","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are defined as RNA transcripts larger than 200 nucleotides that do not appear to have protein-coding potential. Accumulating evidence indicates that lncRNAs are involved in tumorigenesis. Our work reveals that lncRNA FAL1 (focally amplified lncRNA on chromosome 1) is frequently and focally amplified in human cancers and mediates oncogenic functions. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e977154"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.977154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34647762","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}
Justin G Meyerowitz, William A Weiss, W Clay Gustafson
{"title":"A new \"angle\" on kinase inhibitor design: Prioritizing amphosteric activity above kinase inhibition.","authors":"Justin G Meyerowitz, William A Weiss, W Clay Gustafson","doi":"10.4161/23723556.2014.975641","DOIUrl":"https://doi.org/10.4161/23723556.2014.975641","url":null,"abstract":"<p><p>The MYCN oncoprotein has remained an elusive target for decades. We recently reported a new class of kinase inhibitors designed to disrupt the conformation of Aurora kinase A enough to block its kinase-independent interaction with MYCN, resulting in potent degradation of MYCN. These studies provide proof-of-principle for a new method of targeting enzyme activity-independent functions of kinases and other enzymes. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975641"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484597","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":"PKCλ/ι signaling-a common node for normal cellular development and breast oncogenesis.","authors":"Arindam Paul, Soumen Paul","doi":"10.4161/23723556.2014.975076","DOIUrl":"https://doi.org/10.4161/23723556.2014.975076","url":null,"abstract":"<p><p>We recently demonstrated that PKCλ/ι signaling is an important contributor to breast cancer development. Strikingly, PKCλ/ι signaling is also important to balance self-renewal versus differentiation in pluripotent stem cells and is essential for embryonic development. This commentary highlights some key functions of PKCλ/ι signaling that are integral to both normal development and cancer progression. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975076"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484590","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":"A novel miRNA-mediated STOP sign in lung cancer: miR-340 inhibits the proliferation of lung cancer cells through p27(KIP1).","authors":"Serena Fernandez, Maurizio Risolino, Pasquale Verde","doi":"10.4161/23723556.2014.977147","DOIUrl":"https://doi.org/10.4161/23723556.2014.977147","url":null,"abstract":"<p><p>Oncosuppressor miRNAs inhibit cancer cell proliferation by targeting key components of the cell cycle machinery. In our recent report we showed that miR-340 is a novel tumor suppressor in non-small cell lung cancer. miR-340 inhibits neoplastic cell proliferation and induces p27(KIP1) by targeting multiple translational and post-translational regulators of this cyclin-dependent kinase inhibitor. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e977147"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.977147","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34647761","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":"Role of the autonomic nervous system in tumorigenesis and metastasis.","authors":"Claire Magnon","doi":"10.4161/23723556.2014.975643","DOIUrl":"https://doi.org/10.4161/23723556.2014.975643","url":null,"abstract":"<p><p>Convergence of multiple stromal cell types is required to develop a tumorigenic niche that nurtures the initial development of cancer and its dissemination. Although the immune and vascular systems have been shown to have strong influences on cancer, a growing body of evidence points to a role of the nervous system in promoting cancer development. This review discusses past and current research that shows the intriguing role of autonomic nerves, aided by neurotrophic growth factors and axon cues, in creating a favorable environment for the promotion of tumor formation and metastasis. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975643"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975643","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34484599","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":"AMBRA1-induced mitophagy: A new mechanism to cope with cancer?","authors":"Flavie Strappazzon, Francesco Cecconi","doi":"10.4161/23723556.2014.975647","DOIUrl":"https://doi.org/10.4161/23723556.2014.975647","url":null,"abstract":"<p><p>Dysfunctions in mitophagy, the process by which mitochondria are eliminated, are associated with cancer. We found that the proautophagic protein AMBRA1 (activating molecule in beclin 1 regulated autophagy) binds the autophagosome adapter LC3, and that this interaction is crucial for mitochondrial clearance with or without involvement of the E3-ligase PARKIN. The discovery of a novel mitophagy pathway has the potential to promote new anticancer strategies. </p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e975647"},"PeriodicalIF":2.1,"publicationDate":"2015-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.975647","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34647760","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}