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RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0
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RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 13979

Special Issue Editors

Dr. John Murphy

E-Mail Website
Guest Editor
Faculty of Science and Technology, University of Westminster, London, UK
Interests: RNA-binding proteins and cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Kalpana Surendranath

E-Mail Website
Guest Editor
Faculty of Science and Technology, University of Westminster, London, UK
Interests: RNA-DNA damage response and cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Radhakrishnan Kanagaraj

E-Mail Website
Guest Editor
1.School of Life Sciences, University of Westminster, London, UK
2.School of Life Sciences, University of Bedfordshire, Luton, UK
Interests: RNA/DNA secondary structures, genomic instability and human disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The human genome encodes more than 1500 RNA-binding proteins (RBPs), and the number is expected to increase with the addition of RBPs that contain non-canonical RNA binding motifs. These proteins are at the center of transcriptional and post-transcriptional regulation of gene expression and play a central role in all four highly regulated interconnected pathways, namely, transcriptional responses, RNA–DNA damage responses, and DNA repair and apoptosis. Mutations in several RBPs have been linked to cancers, and therefore, RBPs and their associated pathways are potential drug targets. Increasing evidence from research in the past decade highlights the intricate interplay between RNA metabolism, RNA-binding proteins, and genome stability in human health and disease. The proposed issue will broadly cover the following topics:

  • RNA-binding proteins in RNA metabolism;
  • RNA-binding proteins in RNA–DNA damage response;
  • RNA-binding proteins in cancer-associated instability;
  • New technologies to study RNA-binding proteins and RNA/DNA secondary structures;
  • Unresolved RNA/DNA secondary structures and genomic instability.

As Volume 1 of the Special Issue “RNA-Binding Proteins and Their Emerging Roles in Cancer” was particularly successful, we have decided to reopen this issue in the International Journal of Molecular Sciences. This second Special Issue will host review, opinion, and research articles that focus on but are not limited to the above topics.

https://www.mdpi.com/journal/ijms/special_issues/RBPs_cancer

Dr. John Murphy
Dr. Kalpana Surendranath
Dr. Radhakrishnan Kanagaraj
Guest Editors

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 short 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • transcription
  • gene expression
  • RNA splicing
  • RNA editing
  • non-coding RNA
  • R-loop
  • G-quadruplex
  • RNA–DNA damage
  • DNA repair
  • genome instability
  • mutation
  • cancer

Published Papers (5 papers)

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Research

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20 pages, 2159 KiB  
Article
A Degradation Motif in STAU1 Defines a Novel Family of Proteins Involved in Inflammation
by Yulemi Gonzalez Quesada and Luc DesGroseillers
Int. J. Mol. Sci. 2022, 23(19), 11588; https://doi.org/10.3390/ijms231911588 - 30 Sep 2022
Cited by 3 | Viewed by 1728
Abstract
Cancer development is regulated by inflammation. Staufen1 (STAU1) is an RNA-binding protein whose expression level is critical in cancer cells as it is related to cell proliferation or cell death. STAU1 protein levels are downregulated during mitosis due to its degradation by the [...] Read more.
Cancer development is regulated by inflammation. Staufen1 (STAU1) is an RNA-binding protein whose expression level is critical in cancer cells as it is related to cell proliferation or cell death. STAU1 protein levels are downregulated during mitosis due to its degradation by the E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C). In this paper, we map the molecular determinant involved in STAU1 degradation to amino acids 38–50, and by alanine scanning, we shorten the motif to F39PxPxxLxxxxL50 (FPL-motif). Mutation of the FPL-motif prevents STAU1 degradation by APC/C. Interestingly, a search in databases reveals that the FPL-motif is shared by 15 additional proteins, most of them being involved in inflammation. We show that one of these proteins, MAP4K1, is indeed degraded via the FPL-motif; however, it is not a target of APC/C. Using proximity labeling with STAU1, we identify TRIM25, an E3 ubiquitin ligase involved in the innate immune response and interferon production, as responsible for STAU1 and MAP4K1 degradation, dependent on the FPL-motif. These results are consistent with previous studies that linked STAU1 to cancer-induced inflammation and identified a novel degradation motif that likely coordinates a novel family of proteins involved in inflammation. Data are available via ProteomeXchange with the identifier PXD036675. Full article
(This article belongs to the Special Issue RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0)
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18 pages, 3252 KiB  
Article
Phosphomimicry on STAU1 Serine 20 Impairs STAU1 Posttranscriptional Functions and Induces Apoptosis in Human Transformed Cells
by Yulemi Gonzalez Quesada, Florence Bonnet-Magnaval and Luc DesGroseillers
Int. J. Mol. Sci. 2022, 23(13), 7344; https://doi.org/10.3390/ijms23137344 - 1 Jul 2022
Cited by 2 | Viewed by 1529
Abstract
Staufen 1 (STAU1) is an RNA-binding protein that is essential in untransformed cells. In cancer cells, it is rather STAU1 overexpression that impairs cell proliferation. In this paper, we show that a modest increase in STAU1 expression in cancer cells triggers apoptosis as [...] Read more.
Staufen 1 (STAU1) is an RNA-binding protein that is essential in untransformed cells. In cancer cells, it is rather STAU1 overexpression that impairs cell proliferation. In this paper, we show that a modest increase in STAU1 expression in cancer cells triggers apoptosis as early as 12 h post-transfection and impairs proliferation in non-apoptotic cells for several days. Interestingly, a mutation that mimics the phosphorylation of STAU1 serine 20 is sufficient to cause these phenotypes, indicating that serine 20 is at the heart of the molecular mechanism leading to apoptosis. Mechanistically, phosphomimicry on serine 20 alters the ability of STAU1 to regulate translation and the decay of STAU1-bound mRNAs, indicating that the posttranscriptional regulation of mRNAs by STAU1 controls the balance between proliferation and apoptosis. Unexpectedly, the expression of RBD2S20D, the N-terminal 88 amino acids with no RNA-binding activity, is sufficient to induce apoptosis via alteration, in trans, of the posttranscriptional functions of endogenous STAU1. These results suggest that STAU1 is a sensor that controls the balance between cell proliferation and apoptosis, and, therefore, may be considered as a novel therapeutic target against cancer. Full article
(This article belongs to the Special Issue RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0)
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19 pages, 11838 KiB  
Article
Distinct Roles of NANOS1 and NANOS3 in the Cell Cycle and NANOS3-PUM1-FOXM1 Axis to Control G2/M Phase in a Human Primordial Germ Cell Model
by Erkut Ilaslan, Krystyna Kwiatkowska, Maciej Jerzy Smialek, Marcin Piotr Sajek, Zaneta Lemanska, Matisa Alla, Damian Mikolaj Janecki, Jadwiga Jaruzelska and Kamila Kusz-Zamelczyk
Int. J. Mol. Sci. 2022, 23(12), 6592; https://doi.org/10.3390/ijms23126592 - 13 Jun 2022
Cited by 7 | Viewed by 3219
Abstract
Nanos RNA-binding proteins are critical factors of germline development throughout the animal kingdom and their dysfunction causes infertility. During evolution, mammalian Nanos paralogues adopted divergent roles in germ cell biology. However, the molecular basis behind this divergence, such as their target mRNAs, remains [...] Read more.
Nanos RNA-binding proteins are critical factors of germline development throughout the animal kingdom and their dysfunction causes infertility. During evolution, mammalian Nanos paralogues adopted divergent roles in germ cell biology. However, the molecular basis behind this divergence, such as their target mRNAs, remains poorly understood. Our RNA-sequencing analysis in a human primordial germ cell model-TCam-2 cell line revealed distinct pools of genes involved in the cell cycle process downregulated upon NANOS1 and NANOS3 overexpression. We show that NANOS1 and NANOS3 proteins influence different stages of the cell cycle. Namely, NANOS1 is involved in the G1/S and NANOS3 in the G2/M phase transition. Many of their cell cycle targets are known infertility and cancer-germ cell genes. Moreover, NANOS3 in complex with RNA-binding protein PUM1 causes 3′UTR-mediated repression of FOXM1 mRNA encoding a transcription factor crucial for G2/M phase transition. Interestingly, while NANOS3 and PUM1 act as post-transcriptional repressors of FOXM1, FOXM1 potentially acts as a transcriptional activator of NANOS3, PUM1, and itself. Finally, by utilizing publicly available RNA-sequencing datasets, we show that the balance between FOXM1-NANOS3 and FOXM1-PUM1 expression levels is disrupted in testis cancer, suggesting a potential role in this disease. Full article
(This article belongs to the Special Issue RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0)
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Review

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20 pages, 3406 KiB  
Review
R-Loops and R-Loop-Binding Proteins in Cancer Progression and Drug Resistance
by Noha Elsakrmy and Haissi Cui
Int. J. Mol. Sci. 2023, 24(8), 7064; https://doi.org/10.3390/ijms24087064 - 11 Apr 2023
Cited by 6 | Viewed by 4803
Abstract
R-loops are three-stranded DNA/RNA hybrids that form by the annealing of the mRNA transcript to its coding template while displacing the non-coding strand. While R-loop formation regulates physiological genomic and mitochondrial transcription and DNA damage response, imbalanced R-loop formation can be a threat [...] Read more.
R-loops are three-stranded DNA/RNA hybrids that form by the annealing of the mRNA transcript to its coding template while displacing the non-coding strand. While R-loop formation regulates physiological genomic and mitochondrial transcription and DNA damage response, imbalanced R-loop formation can be a threat to the genomic integrity of the cell. As such, R-loop formation is a double-edged sword in cancer progression, and perturbed R-loop homeostasis is observed across various malignancies. Here, we discuss the interplay between R-loops and tumor suppressors and oncogenes, with a focus on BRCA1/2 and ATR. R-loop imbalances contribute to cancer propagation and the development of chemotherapy drug resistance. We explore how R-loop formation can cause cancer cell death in response to chemotherapeutics and be used to circumvent drug resistance. As R-loop formation is tightly linked to mRNA transcription, their formation is unavoidable in cancer cells and can thus be explored in novel cancer therapeutics. Full article
(This article belongs to the Special Issue RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0)
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Other

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12 pages, 2281 KiB  
Perspective
Emerging Roles of NANOS RNA-Binding Proteins in Cancer
by Erkut Ilaslan, Marcin Piotr Sajek, Jadwiga Jaruzelska and Kamila Kusz-Zamelczyk
Int. J. Mol. Sci. 2022, 23(16), 9408; https://doi.org/10.3390/ijms23169408 - 20 Aug 2022
Cited by 5 | Viewed by 1795
Abstract
In recent years, growing evidence demonstrates that mammalian Nanos RNA-binding proteins (Nanos1, Nanos2, and Nanos3), known for their indispensable roles in germline development, are overexpressed in a variety of cancers. This overexpression contributes to various oncogenic properties including cancer growth, invasiveness, and metastasis. [...] Read more.
In recent years, growing evidence demonstrates that mammalian Nanos RNA-binding proteins (Nanos1, Nanos2, and Nanos3), known for their indispensable roles in germline development, are overexpressed in a variety of cancers. This overexpression contributes to various oncogenic properties including cancer growth, invasiveness, and metastasis. Here, we highlight recent findings regarding the role of mammalian Nanos RNA-binding proteins and the mechanisms of their overexpression in cancer. In addition, we present expression profiles of human NANOS genes and their oncogenic transcriptional regulators obtained from publicly available cancer and normal tissue RNA-Seq datasets. Altogether, we emphasize the functional significance of NANOS proteins across human cancers as well as highlight the missing links to understanding the full scope of their role in carcinogenesis. Full article
(This article belongs to the Special Issue RNA-Binding Proteins and Their Emerging Roles in Cancer 2.0)
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