Special Issue "Non-coding RNA and Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (28 February 2013)
Prof. Dr. Peter Zaphiropoulos
Center for Biosciences, Department of Biosciences and Nutrition, Karolinska Institutet, SE-171 77 Stockholm, Sweden
Phone: +46 8 5248 1052
Fax: +46 8 6081 501
Interests: RNA splicing; long non-coding RNAs; miRNAs; RNA editing; genome evolution; Hedgehog signaling; inhibition of tumor growth; oncogenes; tumor suppressor genes
A major challenge in our current understanding of gene expression is the finding that most of the genome is being transcribed. This results in the production of not only mRNAs with protein coding potential but also in a variety of non-coding RNA molecules. One school of thought argues that non-coding RNAs represent errors of the transcriptional apparatus, while others highlight that these molecules may have functional, but sometimes difficult to experimentally define, biological roles. In line with the latter view, evidence is accumulating for the impact of non-coding RNAs in gene transcription, translation, RNA stability, pre-mRNA splicing and chromatin structure. This special issue welcomes manuscripts that address the functional implications of short and long non-coding RNAs, with emphasis on their involvement in disease states and more specifically cancer development.
Prof. Dr. Peter Zaphiropoulos
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- gene transcription
- RNA polymerase
- micro RNA
- long non-coding RNA
- cell proliferation
- tumor growth
- tumor suppressor gene
Cancers 2013, 5(2), 462-490; doi:10.3390/cancers5020462
Received: 1 March 2013; in revised form: 5 April 2013 / Accepted: 19 April 2013 / Published: 26 April 2013| Download PDF Full-text (1061 KB) | Download XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Titel: New Paradigms in ncRNAs as Cancer Therapeutics
Author: Michael Rossbach
Affiliation: Genome Institute of Singapore, 60 Biopolis Street, Singapore 138672, email@example.com
Abstract: RNA interference (RNAi) is triggered by double-stranded RNA (dsRNA) that results in the degradation of homologous mRNA or in the inhibition of mRNA translation. As a basis for differential gene regulation in stem cells, the selective recognition of regulatory DNA sequences is widely accepted. Most transcription factor binding sites, however, are short, degenerate and have a strong affinity for homologous proteins, even ones with antagonistic effects, begging the question “What is regulated in gene regulation?”.
Genome-wide transcription factor binding site studies show that key regulators co-occupy many binding sites. Thus, the prediction of gene activities based on such data is poor. Studies with embryonic stem cells, deficient for dicer (dcr-/-) and targeted with either dcr-1 or dcr-2 from Drosophila melanogaster, give insights into the pathways that underlie the si- and miRNA networks in both wildtype and diseased contexts.
Many of the non-coding transcripts show a differential expression in differentiation and disease and transcriptional interference plays an important role when transcripts compete for transcription. Typical ncRNAs appear to be spliced, polyadenylated, exported just like regular mRNA and processed from longer precursors. Our studies with Dicer give functional insights into the RNA mediated gene silencing pathways and provide novel cellular models for studying the individual effects of ncRNAs, for assay / drug development and biomarker identification. As such, new paradigms in ncRNAs for the development of novel therapeutics for cancer emerge – at the interface of therapy and diagnostics (theranostics), interest has grown in combining both paradigms into clinically effective formulations. NcRNA profiling allows for the identification of specific signatures associated with diagnosis, prognosis, and response to treatment of human diseases and, in particular, tumors. Our cellular models, obtained through the dissection of RNA mediated gene silencing pathways, that can be used for drug screening and biomarker identification are a first step to bringing ncRNAs en route to clinical practice.
Last update: 17 October 2012