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.
Nyitray, Reményi and colleagues (2018), The FEBS Journal
The ERK2-mediated phosphorylation of RSK1, a MAP kinase activated protein kinase, triggers RSK1 activation and subsequent phosphorylation of its substrates including MAG-1. Nyitray, Reményi and colleagues now show that two key residues in the C-terminal tail of RSK1 form an intramolecular and autoregulatory phosphoswitch that dynamically modulates ERK2–RSK1 and RSK1–MAG-1 interactions. Using live-cell imaging, the authors also validate the regulatory role of these interactions in response to growth factor stimulation.
Paterson and Courtneidge (2018), The FEBS Journal
Invadosomes are actin-mediated protrusions that form in cancer cells in response to diverse signalling cues, whereas podosomes are similar structures that form during normal embryonic and post-natal development. In this State-of-the-Art Review, Paterson and Courtneidge highlight the roles of invadosomes and podosomes in normal development, cancer and other diseases, and discuss how these structures could be therapeutically targeted to treat diseases.
D. A. Dougan and colleagues, FEBS Letters
The prokaryotic ubiquitin-like protein (Pup) is a functional analog of ubiquitin in Actinobacteria, and pupylation of proteins via the Pup ligase PafA leads to protein degradation via the bacterial 20S proteasome. Here, free or protein-linked polyPup chains primarily formed through K61 are shown to inhibit proteasomal function. Moreover, autopupylation of PafA in the absence of protein substrates inhibits ligase activity. The authors speculate that this negative feedback loop reversibly controls Pup availability and protein pupylation.
The expression of the embryonic gene Cripto-1 is regulated by OCT4 in human embryonal carcinoma NCCIT cells
J.H. Kim and colleagues, FEBS Letters
Highly malignant embryonal carcinoma (EC) cells maintain self-renewal and differentiation potential and share several signaling pathways with embryonic stem (ES) cells. In this study, Kim J.H. and colleagues show that the Cripto-1 gene, specifically over-expressed in EC and ES cells, is regulated by the transcription factor OCT4 in human EC NCCIT cells. To induce Cripto-1 expression OCT4 was shown to bind specifically to a novel OCT4-binding site within the Cripto-1 minimal promoter region.
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.
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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