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Molecular & Cellular Oncology

Adrian Vallejo, Karmele Valencia, Silvestre Vicent
KRAS proto-oncogene, GTPase (KRAS) remains refractory to current therapies. We devised an integrative cross-tumor approach to expose common core elements up-regulated in mutant KRAS cancers that could provide new treatment opportunities. This approach identified FOSL1 (Fos-like antigen 1) as a clinically and functionally relevant gene in mutant KRAS-driven lung and pancreatic cancers, and unveiled downstream transcriptional targets amenable to pharmacological inhibition.
2017: Molecular & Cellular Oncology
Juan Rodriguez-Vita, Andreas Fischer
Blood vessels supply tumor cells with oxygen and nutrients and provide the basis for metastatic dissemination. In addition, endothelial cells can provide factors that orchestrate the behavior of tumor cells. Here, we expand upon our previous findings that link activation of Notch signaling in the endothelium to cellular senescence, weakening of cell junctions, and expression of adhesion molecules, which facilitates tumor and immune cell migration across the vessel wall and homing at distant sites.
2017: Molecular & Cellular Oncology
Derek J Erstad, Andrew M Tager, Yujin Hoshida, Bryan C Fuchs
Using transcriptome meta-analysis, we recently identified the autotaxin (ATX)-lysophosphatidic acid (LPA) pathway as a regulator of hepatocellular carcinoma (HCC) risk in human cirrhosis patients. Pharmacological targeting of this pathway reduced fibrosis progression and HCC development in animals, identifying ATX-LPA signaling as a novel chemoprevention strategy for cirrhosis and HCC.
2017: Molecular & Cellular Oncology
Shi Hu
Epidermal growth factor receptor (EGFR) is a widely recognized target for tumors, but resistance is commonly reported. Recently, we reported that dual targeting of EGFR and NOTCH2/3 receptors with antibody CT16 showed a strong anti-stem effect both in vitro and in vivo to overcome resistance of EGFR inhibitors and radiation.
2017: Molecular & Cellular Oncology
Yukio Fujiki, Non Miyata, Satoru Mukai, Kanji Okumoto, Emily H Cheng
Loss of voltage-dependent anion channel 2 (VDAC2) leads to impaired peroxisome biogenesis in mammalian cells. Knockdown of BAK restores peroxisomal biogenesis in VDAC2-deficient cells, where BAK localization shifts from mitochondria to peroxisomes. Moreover, overexpression of BAK activators in wild-type cells permeabilizes peroxisomes in a BAK-dependent manner. Together, BAK most likely regulates peroxisomal membrane permeability.
2017: Molecular & Cellular Oncology
Michael C Brown, Matthias Gromeier
mTORC1 is the major homeostatic nutrient sensor for the cell. As such, it is integrated into diverse signaling networks and co-factor interactions that determine its activity. Our recent work implicates the mTORC1 co-factor and PI3K-related Kinase (PIKK) stabilizer, TELO2, in regulating mTORC1 activity in a MAPK-Interacting Kinase (MNK) responsive manner during mitogenic stimulation of cancer cells and T cell activation.
2017: Molecular & Cellular Oncology
Isabelle K Vila, Su Jung Song, Min Sup Song
Ubiquitin-conjugating enzyme E2O (UBE2O) is upregulated in human cancers. We have demonstrated that genetic deletion or pharmacological blockade of UBE2O reduces tumorigenesis through inhibiting the mammalian target of rapamycin complex 1-hypoxia-inducible factor 1-α pathway. Critically, UBE2O targets adenosine monophosphate (AMP)-activated protein kinase-α 2 (AMPKα2) for ubiquitination and degradation. We thus suggest the UBE2O-AMPKα2 axis as a potential therapeutic target for cancer.
2017: Molecular & Cellular Oncology
Mihael Vucur, Anne T Schneider, Jérémie Gautheron, Tom Luedde
Receptor interacting protein kinase 1 (RIPK1) represents a key molecule in cell death. Here, we discuss our recent data on RIPK1 in liver injury and hepatocellular carcinoma development and put these into relation to previous experimental findings to underpin that it exerts opposing kinase-dependent and kinase independent functions in liver cells.
2017: Molecular & Cellular Oncology
Megan Conlon, Scott J Dixon
Ferroptosis is an iron-dependent, oxidative, non-apoptotic form of cell death initially described in mammalian cells. We recently reported that a ferroptosis-like cell death process can be triggered by heat shock in Arabidopsis thaliana. Thus, ferroptosis may be a form of cell death conserved between animals and plants.
2017: Molecular & Cellular Oncology
Hannah Carter, Trey Ideker
Germline variation contributes to individual risk for developing specific types of cancer. Analyzing thousands of tumors, we found evidence that the germline also influences vulnerable tissue sites and the mutations that arise in tumor genomes. These associations provide new clues to unravel the biologic mechanisms underlying cancer predisposition.
2017: Molecular & Cellular Oncology
Marco Demaria
Many genotoxic chemotherapies have debilitating side effects and induce cellular senescence in normal tissues. Senescent cells acquire a pro-inflammatory phenotype which contributes to local and systemic inflammation. Eliminating senescent cells reduce several short- and long-term effects of the drugs, providing a new target to reduce the toxicity of anticancer treatments.
2017: Molecular & Cellular Oncology
Ilio Vitale, Gwenola Manic, Maria Castedo, Guido Kroemer
Mitotic catastrophe is an oncosuppressive mechanism that targets cells experiencing defective mitoses via the activation of specific cell cycle checkpoints, regulated cell death pathways and/or cell senescence. This prevents the accumulation of karyotypic aberrations, which otherwise may drive oncogenesis and tumor progression. Here, we summarize experimental evidence confirming the role of caspase 2 (CASP2) as the main executor of mitotic catastrophe, and we discuss the signals that activate CASP2 in the presence of mitotic aberrations...
2017: Molecular & Cellular Oncology
Victor H Villar, Tra Ly Nguyen, Silvia Terés, Clément Bodineau, Raúl V Durán
A master promoter of cell growth, mammalian target of rapamycin (mTOR) is upregulated in a large percentage of cancer cells. Still, targeting mTOR using rapamycin has a limited outcome in patients. Our recent results highlight the additional role of mTOR as a tumor suppressor, explaining these modest results in the clinic.
2017: Molecular & Cellular Oncology
Zhong Yao, Igor Stagljar
To obtain a global picture of how protein phosphatases are involved in receptor tyrosine kinase (RTK) signaling, we mapped the RTK-phosphatase interactome. Analyses of selected interactions revealed detailed mechanisms of their actions. This study provides new knowledge to better understand cancer development and to identify novel therapeutic targets.
2017: Molecular & Cellular Oncology
Jeff C Kremer, Brian A Van Tine
Argininosuccinate Synthetase 1 deficiency induces dependence on extracellular arginine for continued cellular growth and survival. Arginine starvation inhibits the Warburg effect and diverts glucose into serine biosynthesis, while simultaneously increasing glutamine metabolism via the tricarboxylic acid cycle. Simultaneous arginine deprivation and inhibition of the subsequent metabolic adaptations induce synthetic lethality.
2017: Molecular & Cellular Oncology
Atif A Ahmed, Abdalla D Mohamed, Melissa Gener, Weijie Li, Eugenio Taboada
The Hippo pathway is an important signaling pathway that controls cell proliferation and apoptosis. It is evolutionarily conserved in mammals and is stimulated by cell-cell contact, inhibiting cell proliferation in response to increased cell density. During early embryonic development, the Hippo signaling pathway regulates organ development and size, and its functions result in the coordinated balance between proliferation, apoptosis, and differentiation. Its principal effectors, YAP and TAZ, regulate signaling by the embryonic stem cells and determine cell fate and histogenesis...
2017: Molecular & Cellular Oncology
Chaoqun Li, Wei Yu
Aminoacyl-tRNA synthetases, catalyzing the first step of protein synthesis, have been shown to involve with multiple additional physiologic responses. Here, we summarize our findings that p300/CBP-Associated Factor and Sirtuin 1 play the reversible acetylation role in regulating the nuclear translocation of Tyrosyl-tRNA synthetase and activating transcription factor E2F1, thus facilitating the repair of damaged DNA.
2017: Molecular & Cellular Oncology
S Hoffmann, D Fachinetti
Proper chromosome segregation relies on a functional centromere-kinetochore interface. We showed that chromatin containing CENtromere Protein A (CENP-A) is essential for centromere assembly, but dispensable for chromosome segregation in the presence of CENP-B-bound DNA sequences. This demonstrates the existence of two contact points between the DNA and the kinetochore to mediate successful chromosome segregation.
2017: Molecular & Cellular Oncology
Kristine M Wadosky, Leigh Ellis, David W Goodrich
Prostate cancer variants expressing alternative lineage markers appear at relapse from antiandrogen therapy. We show that loss of the retinoblastoma (RB1) and tumor protein 53 (TP53) genes drives expression of stem cell reprogramming factors, lineage plasticity, and antiandrogen resistance. Epigenetic manipulation restores antiandrogen sensitivity-suggesting an approach for treating lethal prostate cancers.
2017: Molecular & Cellular Oncology
Stefanie Göllner, Carsten Müller-Tidow
The polycomb protein enhancer of zeste homolog 2 (EZH2) may have a dual role in cancer pathogenesis acting as an oncogene or as a tumor suppressor depending on the cancer type. We recently demonstrated that proteasomal degradation of EZH2 resulting from cyclin-dependent kinase 1 (CDK1)-induced phosphorylation at Threonine (T) 487 represents a novel mechanism of drug resistance in acute myeloid leukemia (AML). Our findings suggest that restoration of EZH2 protein is a viable approach to overcome therapy resistance in AML...
2017: Molecular & Cellular Oncology
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