Involvement of RNA Polymerases I and III in Cancer Progression (Volume II)

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 21 March 2025 | Viewed by 1700

Special Issue Editor


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Guest Editor
Department of Biology, University of York, York YO10 5DD, UK
Interests: cancer; industrial biotechnology; RNA polymerase III; transcription; tRNA genes
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Special Issue Information

Dear Colleagues,

We are excited to invite you to contribute to this Special Issue, which is the second edition of "Involvement of RNA Polymerases I and III in Cancer Progression" (https://www.mdpi.com/journal/cancers/special_issues/RNAIAIII).

The active synthesis of rRNA and tRNA by RNA polymerases (pols) I and III is a fundamental determinant of a cell’s capacity to grow. Most if not all cancers are likely to express abnormal levels of rRNAs and tRNAs. Multiple molecular mechanisms have been shown to contribute to this deregulation, including the aberrant expression of specific transcription factors, the activation of oncogenic signalling pathways, direct targeting by oncogene products, and the loss of restraint by key tumour suppressors. Far less is known about the consequences of these changes, although a growing body of evidence has implicated specific tRNAs in promoting metastasis. Furthermore, the deep sequencing of cancer genomes on a massive scale has implicated in tumorigenesis several other noncoding RNA genes that are transcribed by pol III, such as the RMRP gene. Strategies to manipulate pol III as a therapeutic target remain at early preclinical stages, but a specific inhibitor of pol I has reached clinical trials for solid and haematological malignancies.

This Special Issue aims to consider the involvement of pols I and III in cancer initiation, progression, and maintenance, including the roles of their individual ncRNA products. Related topics of interest include the molecular mechanisms responsible for the aberrant function of pols I and III in tumours and the potential of targeting these essential enzymes for therapeutic intervention.

Prof. Dr. Robert J. White
Guest Editor

Manuscript Submission Information

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. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (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 thoroughly refereed through a single-blind 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 semimonthly 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 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer
  • RNA polymerase I
  • RNA polymerase III
  • rRNA
  • tRNA

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Published Papers (1 paper)

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Research

21 pages, 5776 KiB  
Article
Selective Occupation by E2F and RB of Loci Expressed by RNA Polymerase III
by Rebecca E. Sizer, Sienna P. Butterfield, Lucy A. Hancocks, Leonor Gato De Sousa and Robert J. White
Cancers 2024, 16(3), 481; https://doi.org/10.3390/cancers16030481 - 23 Jan 2024
Cited by 1 | Viewed by 1480
Abstract
In all cases tested, TFIIIB is responsible for recruiting pol III to its genetic templates. In mammalian cells, RB binds TFIIIB and prevents its interactions with both promoter DNA and pol III, thereby suppressing transcription. As TFIIIB is not recruited to its target [...] Read more.
In all cases tested, TFIIIB is responsible for recruiting pol III to its genetic templates. In mammalian cells, RB binds TFIIIB and prevents its interactions with both promoter DNA and pol III, thereby suppressing transcription. As TFIIIB is not recruited to its target genes when bound by RB, the mechanism predicts that pol III-dependent templates will not be occupied by RB; this contrasts with the situation at most genes controlled by RB, where it can be tethered by promoter-bound sequence-specific DNA-binding factors such as E2F. Contrary to this prediction, however, ChIP-seq data reveal the presence of RB in multiple cell types and the related protein p130 at many loci that rely on pol III for their expression, including RMRP, RN7SL, and a variety of tRNA genes. The sets of genes targeted varies according to cell type and growth state. In such cases, recruitment of RB and p130 can be explained by binding of E2F1, E2F4 and/or E2F5. Genes transcribed by pol III had not previously been identified as common targets of E2F family members. The data provide evidence that E2F may allow for the selective regulation of specific non-coding RNAs by RB, in addition to its influence on overall pol III output through its interaction with TFIIIB. Full article
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