FEBS Press is pleased to welcome its fourth journal, Molecular Oncology, to this platform. Molecular Oncology is now fully Open Access and all content from the past 10 years is now available for all to read. The publication of high-quality journals by scientists for scientists is one the core objectives of The Federation of European Biochemical Societies (FEBS), with the revenue raised supporting fellowships, courses, congresses and other activities.

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The FEBS Journal For high-quality full-length papers and reviews, with particular focus on biochemistry, molecular biology, structural biology and cell biology.
FEBS Letters For highly significant research letters that merit urgent publication, as well as timely reviews of wide interest in the molecular biosciences.
Molecular OncologyFor high-impact discoveries, approaches and technical advances in basic, clinical and discovery-driven translational cancer research.
FEBS Open Bio For rapid open access publication of scientifically sound research articles in the molecular and cellular life sciences.

Highlighted Articles

Metabolic reprogramming and epithelial-to-mesenchymal transition in cancer

Sciacovelli and Frezza (2017), The FEBS Journal

Epithelial-to-mesenchymal transition (EMT) is a process whereby epithelial cancer cells can acquire mesenchymal features allowing them to migrate and invade other tissues, thus enabling tumour metastasis. In this State-of-the-Art Review, Sciacovelli and Frezza discuss the molecular underpinnings of metabolic reprogramming during EMT and how in some instances deregulation of metabolic pathways could drive EMT.

Mapping the interactome of HPV E6 and E7 oncoproteins with the ubiquitin-proteasome system

Masson and colleagues (2017), The FEBS Journal

The Ubiquitin Proteasome System (UPS) regulates protein homeostasis and is targeted by viruses to enhance viral replication and escape host immune responses. Masson and colleagues assembled and screened a library of 590 cDNAs encoding UPS factors for binary interactions with human papillomavirus 16 (HPV16) E6 and E7 proteins using the Gaussia princeps luciferase complementation assay. This study identified ubiquitin ligases and deubiquitinases targeted by viral E6 and E7, and established a system for rapid identification of host or pathogen proteins that interact with the UPS.

An engineered photoswitchable mammalian pyruvate kinase

Anastasiou and colleagues, The FEBS Journal

The glycolytic enzyme pyruvate kinase M2 (PKM2) plays a pivotal role in cancer metabolism and is allosterically activated by a variety of ligands. Whether this allosteric regulation impacts cell proliferation is still unclear. Anastasiou and colleagues engineered a photoswitchable PKM2 variant through insertion of the light/oxygen/voltage-sensitive domain 2 (LOV2) into a ligand binding domain. The resulting chimeric protein undergoes light-induced conformational changes, leading to an increase in pyruvate kinase activity. The photoswitchable PKM2 is a useful tool for studying the impact of allosteric regulation on metabolism and cell proliferation.  

ADP-ribosylation: new facets of an ancient modification 

Ahel and colleagues, The FEBS Journal

ADP-ribosylation is a conserved chemical modification involved in the regulation of many cellular processes, including DNA damage repair, transcription and cell cycle progression. This State-of-the-Art Review by Ahel and colleagues presents the latest advances on the ADP-ribosylation machinery in eukaryotes, bacteria and viruses and the newly discovered pathways regulated by ADP-ribosylation.

Rothman and colleagues

ACBD3 functions as a scaffold to organize the Golgi stacking proteins and a Rab33b-GAP

Rothman,Qian, Lee and colleagues, FEBS Letters

Golgi tethers, such as Golgin45, and GRASP proteins, such as GRASP55, stack Golgi cisternae together. A proteomic analysis has identified ACBD3 (which was previously shown to bind the Golgin tether Giantin) as a scaffold protein that recruits Golgin45 to a Golgin45–GRASP55-containing cisternal adhesion complex. ACBD3 also recruits the Rab33b GTPase-activating protein TBC1D22 to the complex. The authors suggest cisternal adhesion complexes may include more proteins than previously anticipated and also regulate the membrane dynamics of Rab-GTPases at the medial Golgi.

Teis and colleagues

Regulation of Rab5 isoforms by transcriptional and post-transcriptional mechanisms in yeast

Teis and colleagues, FEBS Letters

Yeast encodes three isoforms of the endosome biogenesis regulator Rab5. Vps21, the most abundantly expressed Rab5, is sufficient to maintain endosomal function. Ypt53, the least abundant isoform, fails to fully rescue cell growth in Vps21 mutants. Here, Ypt53 expression is shown to be repressed through mRNA decay. Nutrient starvation or endosomal dysfunction partially increased Ypt53 expression through activity of the transcription factors Gis1 and Crz1. Ypt53 could only restore endosomal functions, once it was exogenously expressed to an even higher level.

Indoxyl sulfate

A uremic toxin (indoxyl sulfate) found in chronic kidney disease supresses bone formation and resorption

Inada and colleagues, FEBS Open Bio

Patients with chronic kidney disease (CKD) often present with bone turnover abnormalities, which has been associated with low serum levels of parathyroid hormone (PTH). Here, Inada and colleagues report that Indoxyl sulphate (IS), a uremic toxin known to accumulate in the blood of CKD patients, directly supresses osteoblast/osteoclast coupling and bone formation in vitro. This, combined with their previous findings that showed IS exacerbated low bone turnover induced by parathyroidectomy suggests that IS directly induces low bone turnover via the inhibition of bone formation using mechanisms separate from skeletal resistance to parathyroid hormone (PTH). This suggests IS initiates low-turnover bone disease in patients with CKD via a direct action upon both osteoclast precursors and osteoblasts to supress bone formation and resorption.


Dovitinib enhances temozolomide efficacy in glioblastoma cells

Hombach-Klonisch and colleagues, Molecular Oncology

Dovitinib (Dov), an FDA- approved oral drug, is able to cross the blood-brain barrier and has recently demonstrated promising efficacy in clinical trials for glioblastoma (GB) patients with recurrent disease. The Dov-mediated molecular mechanisms in GB cells remained unknown. Here, Hombach-Klonisch and colleagues show that Dov treatment attenuated the STAT3/LIN28/Let-7/HMGA2 regulatory axis in GB cells, and downregulated key base excision repair factors known to repair temozolomide (TMZ) induced DNA damage. Dual or sequential treatment with Dov and TMZ enhanced the efficacy of TMZ, reduced GB cell survival, growth, and self-renewal capacity and severely compromised the recovery of GB cells. Alternate administration of Dov and TMZ may improve therapeutic efficacy, especially in patients expected to exhibit increased TMZ resistance. These findings suggest ‘Dov priming’ is an encouraging novel therapeutic strategy to improve the efficacy of TMZ in patients with GB.

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