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Cancers
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Ribosomes in Cancer
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Ribosomes in Cancer

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

Deadline for manuscript submissions: closed (10 March 2022) | Viewed by 19604

Special Issue Editors

Dr. Jean Jacques Diaz

E-Mail Website
Guest Editor
Centre de Recherche en Cancérologie de Lyon, UMR Inserm 1052 - CNRS 5286 - UCBL-CLB, 28, rue Laennec, 69008 Lyon, France
Interests: ribosome; specialized ribosome; chemical modification of rRNA; 2’-O-methylation; rRNA epitranscriptome; translation; cancer; therapy; biomarkers
Dr. Virginie Marcel

E-Mail Website
Co-Guest Editor
Centre de Recherche en Cancérologie de Lyon, UMR Inserm 1052 - CNRS 5286 - UCBL-CLB, 28, rue Laennec, 69008 Lyon, France
Interests: ribosome; specialized ribosome; chemical modification of rRNA; 2’-O-methylation; rRNA epitranscriptome; translation; cancer; therapy; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Frédéric Catez

E-Mail Website
Co-Guest Editor
Centre de Recherche en Cancérologie de Lyon, UMR Inserm 1052 - CNRS 5286 - UCBL-CLB, 28, rue Laennec, 69008 Lyon, France
Interests: ribosome; specialized ribosome; chemical modification of rRNA; 2’-O-methylation; rRNA epitranscriptome; translation; cancer; therapy; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Ribosomes are at the heart of gene expression, translating all cellular mRNAs into proteins. Cells have the potential to produce a myriad of ribosomes through genetic variants and chemical modifications of the 4 RNAs and 80 proteins that comprise human ribosomes. In the last decade, basic and translational studies have brought to light the contribution of ribosome activity in acquisition of the cancer hallmarks of tumor cells that are driven by profound translational reprogramming, and unveiled the potential of targeting ribosomes in cancer therapy.

The Special Issue “Ribosomes in Cancer” aims at compiling these novel and exciting discoveries to consolidate the place of the human ribosome as a key biological object in oncology—not only to better understand cancer biology but also to promote usage of ribosomes in clinic as a biomarker and therapeutic target.

Dr. Jean Jacques Diaz
Dr. Frédéric Catez
Dr. Virginie Marcel
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 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

  • ribosome
  • ribosomal protein
  • ribosomal RNA
  • mutation
  • chemical modification
  • translation
  • tumorigenesis
  • cancer progression
  • therapy, biomarkers

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Published Papers (5 papers)

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Research

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16 pages, 4065 KiB  
Article
Frequent 4EBP1 Amplification Induces Synthetic Dependence on FGFR Signaling in Cancer
by Prathibha Mohan, Joyce Pasion, Giovanni Ciriello, Nathalie Lailler, Elisa de Stanchina, Agnes Viale, Anke van den Berg, Arjan Diepstra, Hans-Guido Wendel, Viraj R. Sanghvi and Kamini Singh
Cancers 2022, 14(10), 2397; https://doi.org/10.3390/cancers14102397 - 13 May 2022
Cited by 1 | Viewed by 3246
Abstract
The eIF4E translation initiation factor has oncogenic properties and concordantly, the inhibitory eIF4E-binding protein (4EBP1) is considered a tumor suppressor. The exact molecular effects of 4EBP1 activation in cancer are still unknown. Surprisingly, 4EBP1 is a target of genomic copy number gains (Chr. [...] Read more.
The eIF4E translation initiation factor has oncogenic properties and concordantly, the inhibitory eIF4E-binding protein (4EBP1) is considered a tumor suppressor. The exact molecular effects of 4EBP1 activation in cancer are still unknown. Surprisingly, 4EBP1 is a target of genomic copy number gains (Chr. 8p11) in breast and lung cancer. We noticed that 4EBP1 gains are genetically linked to gains in neighboring genes, including WHSC1L1 and FGFR1. Our results show that FGFR1 gains act to attenuate the function of 4EBP1 via PI3K-mediated phosphorylation at Thr37/46, Ser65, and Thr70 sites. This implies that not 4EBP1 but instead FGFR1 is the genetic target of Chr. 8p11 gains in breast and lung cancer. Accordingly, these tumors show increased sensitivity to FGFR1 and PI3K inhibition, and this is a therapeutic vulnerability through restoring the tumor-suppressive function of 4EBP1. Ribosome profiling reveals genes involved in insulin signaling, glucose metabolism, and the inositol pathway to be the relevant translational targets of 4EBP1. These mRNAs are among the top 200 translation targets and are highly enriched for structure and sequence motifs in their 5′UTR, which depends on the 4EBP1-EIF4E activity. In summary, we identified the translational targets of 4EBP1-EIF4E that facilitate the tumor suppressor function of 4EBP1 in cancer. Full article
(This article belongs to the Special Issue Ribosomes in Cancer)
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18 pages, 4639 KiB  
Article
Synergy of Venetoclax and 8-Chloro-Adenosine in AML: The Interplay of rRNA Inhibition and Fatty Acid Metabolism
by Dinh Hoa Hoang, Corey Morales, Ivan Rodriguez Rodriguez, Melissa Valerio, Jiamin Guo, Min-Hsuan Chen, Xiwei Wu, David Horne, Varsha Gandhi, Lisa S. Chen, Bin Zhang, Vinod Pullarkat, Steven T. Rosen, Guido Marcucci, Ralf Buettner and Le Xuan Truong Nguyen
Cancers 2022, 14(6), 1446; https://doi.org/10.3390/cancers14061446 - 11 Mar 2022
Cited by 9 | Viewed by 2724
Abstract
It is known that 8-chloro-adenosine (8-Cl-Ado) is a novel RNA-directed nucleoside analog that targets leukemic stem cells (LSCs). In a phase I clinical trial with 8-Cl-Ado in patients with refractory or relapsed (R/R) AML, we observed encouraging but short-lived clinical responses, likely due [...] Read more.
It is known that 8-chloro-adenosine (8-Cl-Ado) is a novel RNA-directed nucleoside analog that targets leukemic stem cells (LSCs). In a phase I clinical trial with 8-Cl-Ado in patients with refractory or relapsed (R/R) AML, we observed encouraging but short-lived clinical responses, likely due to intrinsic mechanisms of LSC resistance. LSC homeostasis depends on amino acid-driven and/or fatty acid oxidation (FAO)-driven oxidative phosphorylation (OXPHOS) for survival. We recently reported that 8-Cl-Ado and the BCL-2-selective inhibitor venetoclax (VEN) synergistically inhibit FAO and OXPHOS in LSCs, thereby suppressing acute myeloid leukemia (AML) growth in vitro and in vivo. Herein, we report that 8-Cl-Ado inhibits ribosomal RNA (rRNA) synthesis through the downregulation of transcription initiation factor TIF-IA that is associated with increasing levels of p53. Paradoxically, 8-Cl-Ado-induced p53 increased FAO and OXPHOS, thereby self-limiting the activity of 8-Cl-Ado on LSCs. Since VEN inhibits amino acid-driven OXPHOS, the addition of VEN significantly enhanced the activity of 8-Cl-Ado by counteracting the self-limiting effect of p53 on FAO and OXPHOS. Overall, our results indicate that VEN and 8-Cl-Ado can cooperate in targeting rRNA synthesis and OXPHOS and in decreasing the survival of the LSC-enriched cell population, suggesting the VEN/8-Cl-Ado regimen as a promising therapeutic approach for patients with R/R AML. Full article
(This article belongs to the Special Issue Ribosomes in Cancer)
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18 pages, 2922 KiB  
Article
Translational Regulation by hnRNP H/F Is Essential for the Proliferation and Survival of Glioblastoma
by Morgane Le Bras, Noah Gorelick, Sylvain Pautet, Betty Tyler, Stéphane Manenti, Nicolas Skuli, Stefania Millevoi and Anne Cammas
Cancers 2022, 14(5), 1283; https://doi.org/10.3390/cancers14051283 - 2 Mar 2022
Cited by 5 | Viewed by 2749
Abstract
Deregulation of mRNA translation is a widespread characteristic of glioblastoma (GBM), aggressive malignant brain tumors that are resistant to conventional therapies. RNA-binding proteins (RBPs) play a critical role in translational regulation, yet the mechanisms and impact of these regulations on cancer development, progression [...] Read more.
Deregulation of mRNA translation is a widespread characteristic of glioblastoma (GBM), aggressive malignant brain tumors that are resistant to conventional therapies. RNA-binding proteins (RBPs) play a critical role in translational regulation, yet the mechanisms and impact of these regulations on cancer development, progression and response to therapy remain to be fully understood. Here, we showed that hnRNP H/F RBPs are potent regulators of translation through several mechanisms that converge to modulate the expression and/or the activity of translation initiation factors. Among these, hnRNP H/F regulate the phosphorylation of eIF4E and its translational targets by controlling RNA splicing of the A-Raf kinase mRNA, which in turn modulates the MEK-ERK/MAPK signaling pathway. The underlying mechanism involves RNA G-quadruplex (RG4s), RNA structures whose modulation phenocopies hnRNP H/F translation regulation in GBM cells. Our results highlighted that hnRNP H/F are essential for key functional pathways regulating proliferation and survival of GBM, highlighting its targeting as a promising strategy for improving therapeutic outcomes. Full article
(This article belongs to the Special Issue Ribosomes in Cancer)
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Review

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14 pages, 1120 KiB  
Review
Targeting Ribosome Biogenesis to Combat Tamoxifen Resistance in ER+ve Breast Cancer
by Ho Tsoi, Chan-Ping You, Man-Hong Leung, Ellen P. S. Man and Ui-Soon Khoo
Cancers 2022, 14(5), 1251; https://doi.org/10.3390/cancers14051251 - 28 Feb 2022
Cited by 13 | Viewed by 3345
Abstract
Breast cancer is a heterogeneous disease. Around 70% of breast cancers are estrogen receptor-positive (ER+ve), with tamoxifen being most commonly used as an adjuvant treatment to prevent recurrence and metastasis. However, half of the patients will eventually develop tamoxifen resistance. The overexpression of [...] Read more.
Breast cancer is a heterogeneous disease. Around 70% of breast cancers are estrogen receptor-positive (ER+ve), with tamoxifen being most commonly used as an adjuvant treatment to prevent recurrence and metastasis. However, half of the patients will eventually develop tamoxifen resistance. The overexpression of c-MYC can drive the development of ER+ve breast cancer and confer tamoxifen resistance through multiple pathways. One key mechanism is to enhance ribosome biogenesis, synthesising mature ribosomes. The over-production of ribosomes sustains the demand for proteins necessary to maintain a high cell proliferation rate and combat apoptosis induced by therapeutic agents. c-MYC overexpression can induce the expression of eIF4E that favours the translation of structured mRNA to produce oncogenic factors that promote cell proliferation and confer tamoxifen resistance. Either non-phosphorylated or phosphorylated eIF4E can mediate such an effect. Since ribosomes play an essential role in c-MYC-mediated cancer development, suppressing ribosome biogenesis may help reduce aggressiveness and reverse tamoxifen resistance in breast cancer. CX-5461, CX-3543 and haemanthamine have been shown to repress ribosome biogenesis. Using these chemicals might help reverse tamoxifen resistance in ER+ve breast cancer, provided that c-MYC-mediated ribosome biogenesis is the crucial factor for tamoxifen resistance. To employ these ribosome biogenesis inhibitors to combat tamoxifen resistance in the future, identification of predictive markers will be necessary. Full article
(This article belongs to the Special Issue Ribosomes in Cancer)
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19 pages, 4254 KiB  
Review
Inhibition of the Eukaryotic 80S Ribosome as a Potential Anticancer Therapy: A Structural Perspective
by Simone Pellegrino, Salvatore Terrosu, Gulnara Yusupova and Marat Yusupov
Cancers 2021, 13(17), 4392; https://doi.org/10.3390/cancers13174392 - 31 Aug 2021
Cited by 6 | Viewed by 6345
Abstract
Protein biosynthesis is a vital process for all kingdoms of life. The ribosome is the massive ribonucleoprotein machinery that reads the genetic code, in the form of messenger RNA (mRNA), to produce proteins. The mechanism of translation is tightly regulated to ensure that [...] Read more.
Protein biosynthesis is a vital process for all kingdoms of life. The ribosome is the massive ribonucleoprotein machinery that reads the genetic code, in the form of messenger RNA (mRNA), to produce proteins. The mechanism of translation is tightly regulated to ensure that cell growth is well sustained. Because of the central role fulfilled by the ribosome, it is not surprising that halting its function can be detrimental and incompatible with life. In bacteria, the ribosome is a major target of inhibitors, as demonstrated by the high number of small molecules identified to bind to it. In eukaryotes, the design of ribosome inhibitors may be used as a therapy to treat cancer cells, which exhibit higher proliferation rates compared to healthy ones. Exciting experimental achievements gathered during the last few years confirmed that the ribosome indeed represents a relevant platform for the development of anticancer drugs. We provide herein an overview of the latest structural data that helped to unveil the molecular bases of inhibition of the eukaryotic ribosome triggered by small molecules. Full article
(This article belongs to the Special Issue Ribosomes in Cancer)
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