Gerardo Ferbeyre

Université de Montréal

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Véronique Bourdeau

Université de Montréal

Frédéric Lessard

Université de Sherbrooke

Xavier Deschênes‐Simard

Memorial Sloan Kettering Cancer Center

Lian Mignacca

Université de Montréal

Marie‐Camille Rowell

Cancer Institute (WIA)

Sebastian Igelmann

VIB-KU Leuven Center for Cancer Biology

Geneviève Huot

Université de Montréal

Subburaj Ilangumaran

Université de Sherbrooke

Mathieu Vernier

Centre de Recherche en Cancérologie de Lyon

Olga Moiseeva

G. K. Skryabin Institute of Biochemistry and Physiology of Microorganisms

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Université de Montréal

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McGill University

131

Université de Sherbrooke

McGill University Health Centre

Inserm

Centre National de la Recherche Scientifique

Institute for Research in Immunology and Cancer

Jewish General Hospital

Centre Hospitalier de l’Université de Montréal

Montreal Heart Institute

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Endogenous oxidative stress prevents telomerase-dependent immortalization of human endothelial cells

Mechanisms of Ageing and Development (2010)

Guillaume Voghel Nathalie Thorin‐Trescases Aida M. Mamarbachi Louis Villeneuve Frédérick A. Mallette

Senescence

10.1016/j.mad.2010.04.004

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Citations (34)

Supplementary data-G&D(6)

Xavier Deschênes‐Simard Marie‐France Gaumont‐Leclerc Véronique Bourdeau Frédéric Lessard О. М. Моисеева

Source

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Distribution of Hammerhead and Hammerhead-like RNA Motifs Through the GenBank

Genome Research (2000)

Gerardo Ferbeyre Véronique Bourdeau M. Pageau Pedro Miramóntes Robert Cedergren

Hammerhead ribozymes previously were found in satellite RNAs from plant viroids and in repetitive DNA from certain species of newts and schistosomes. To determine if this catalytic RNA motif has a wider distribution, we decided to scrutinize the GenBank database for RNAs that contain hammerhead or hammerhead-like motifs. The search shows a widespread distribution of this kind of RNA motif in different sequences suggesting that they might have a more general role in RNA biology. The frequency of the hammerhead motif is half of that expected from a random distribution, but this fact comes from the low CpG representation in vertebrate sequences and the bias of the GenBank for those sequences. Intriguing motifs include those found in several families of repetitive sequences, in the satellite RNA from the carrot red leaf luteovirus, in plant viruses like the spinach latent virus and the elm mottle virus, in animal viruses like the hepatitis E virus and the caprine encephalitis virus, and in mRNAs such as those coding for cytochrome P450 oxidoreductase in the rat and the hamster.

Hammerhead ribozyme

10.1101/gr.10.7.1011

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Figure S3 from The Role of HMGB1 in Radioresistance of Bladder Cancer

Sanhita Shrivastava José João Mansure Wael Almajed Fabio Cury Gerardo Ferbeyre

<p>UM-UC5 Comet Assay Results</p>

Radioresistance

10.1158/1535-7163.22503831

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Senescent Macrophages Release Inflammatory Cytokines and RNA-Loaded Extracellular Vesicles to Circumvent Fibroblast Senescence

Biomedicines (2024)

Camille Laliberté Bianca Bossé Véronique Bourdeau Luis I. Prieto Genève Perron-Deshaies

Senescent cells, which accumulate with age, exhibit a pro-inflammatory senescence-associated secretory phenotype (SASP) that includes the secretion of cytokines, lipids, and extracellular vesicles (EVs). Here, we established an in vitro model of senescence induced by Raf-1 oncogene in RAW 264.7 murine macrophages (MΦ) and compared them to senescent MΦ found in mouse lung tumors or primary macrophages treated with hydrogen peroxide. The transcriptomic analysis of senescent MΦ revealed an important inflammatory signature regulated by NFkB. We observed an increased secretion of EVs in senescent MΦ, and these EVs presented an enrichment for ribosomal proteins, major vault protein, pro-inflammatory miRNAs, including miR-21a, miR-155, and miR-132, and several mRNAs. The secretion of senescent MΦ allowed senescent murine embryonic fibroblasts to restart cell proliferation. This antisenescence function of the macrophage secretome may explain their pro-tumorigenic activity and suggest that senolytic treatment to eliminate senescent MΦ could potentially prevent these deleterious effects.

Senescence

Proinflammatory cytokine

10.3390/biomedicines12051089

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An E2F/miR-20a Autoregulatory Feedback Loop

Journal of Biological Chemistry (2006)

Yannick Sylvestre Vincent De Guire Emmanuelle Querido Utpal K. Mukhopadhyay Véronique Bourdeau

The E2F family of transcription factors is essential in the regulation of the cell cycle and apoptosis. While the activity of E2F1-3 is tightly controlled by the retinoblastoma family of proteins, the expression of these factors is also regulated at the level of transcription, post-translational modifications and protein stability. Recently, a new level of regulation of E2Fs has been identified, where micro-RNAs (miRNAs) from the mir-17-92 cluster influence the translation of the E2F1 mRNA. We now report that miR-20a, a member of the mir-17-92 cluster, modulates the translation of the E2F2 and E2F3 mRNAs via binding sites in their 3'-untranslated region. We also found that the endogenous E2F1, E2F2, and E2F3 directly bind the promoter of the mir-17-92 cluster activating its transcription, suggesting an autoregulatory feedback loop between E2F factors and miRNAs from the mir-17-92 cluster. Our data also point toward an anti-apoptotic role for miR-20a, since overexpression of this miRNA decreased apoptosis in a prostate cancer cell line, while inhibition of miR-20a by an antisense oligonucleotide resulted in increased cell death after doxorubicin treatment. This anti-apoptotic role of miR-20a may explain some of the oncogenic capacities of the mir-17-92 cluster. Altogether, these results suggest that the autoregulation between E2F1-3 and miR-20a is important for preventing an abnormal accumulation of E2F1-3 and may play a role in the regulation of cellular proliferation and apoptosis.

Feedback loop

Negative feedback

10.1074/jbc.m608939200

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Citations (606)

Transcripts from S chistosom a Nonautonomous Retrotransposons Possess Catalytic A c tiv ity

CRC Press eBooks (2009)

Gerardo Ferbeyre

Eukaryotic genomes are largely shaped by the presence of multiple mobile elements. A large fraction of these sequences carry a double life, alternating between DNA and RNA through the process of transcription and reverse transcription. The presence of mobile elements in eukaryotic genomes is potentially deleterious since they inactivate genes or change their expression. However, they also provide a source of variation for natural selection to act. Over the last decade we have learned that RNA molecules not only serve as messengers of the information content in DNA. RNA can have a variety of functions including the ability to catalyze chemical reactions. RNA molecules with catalytic activity are known as ribozymes and were originally found in self-splicing introns, the RNA subunit of RNase P and certain plant viroids and their satellite RNAs. The catalytic motif present in viroids was dubbed hammer head due to the apparent shape of its secondary structure. Viroids use the hammerhead self-cleavage reaction to process the multimeric intermediates of their rolling-circle replication. Surprisingly, some repetitive elements discovered in the newt, schistosomes and crickets also encode hammerhead ribozymes. In schistosomes, the Sm a family of nonautonomous retrotransposons apparendy use the self-cleavage reaction to process the multimeric transcripts arising from transcription of tandem repeats. Apart from processing, this self-cleavage reaction could limit retrotransposons propagation, representing a novel mechanism of host protection against these genomic parasites. In addition, the Sma ribozymes can potentially catalyze RNA cleavage in trans as demonstrated in vitro for the mRNA coding for synaptobrevin. Other substrates predicted for the Sma ribozyme such as multimeric transcripts from Sm a repeats containing mutated hammerhead motifs, the mRNA coding for a nuclear receptor like protein and the OZ retrotransposons require further study.

Retrotransposon

10.1201/9781498712880-6

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Bile acids in the fountain of youth

Aging (2010)

Gerardo Ferbeyre

Anyone lucky enough to drink water from the fountain of youth could retard its aging process, as the legend tells.Most likely, water was not the only element in the legendary fountain.What else could be found in there?We may never know!But scientists could come across their own anti-aging ingredients using model organisms and collections of chemical compounds, as the Titorenko's lab reports in this issue of Aging.

Fountain

10.18632/aging.100169

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Transcriptome analysis and tumor suppressor requirements of STAT5‐induced senescence

Annals of the New York Academy of Sciences (2010)

Frédérick A. Mallette Olga Moiseeva Viviane Calabrese Botum Mao Marie‐France Gaumont‐Leclerc

Although it is acknowledged that senescent cells accumulate with age, the molecular mechanisms leading to cell senescence as a function of age remain to be identified. In cell culture models, it has been clearly shown that senescence involves the activation of a DNA damage response secondary to short telomeres or oncogene expression. Oncogenes are altered versions of genes coding for proteins that mediate signals from extracellular factors such as cytokines, growth factors, and hormones. In particular, we show here that constitutive activation of the JAK/STAT5 signaling pathway induces senescence in both mouse and human normal cells. The process involves activation of the p53 and Rb tumor suppressor pathways and mitochondrial dysfunction. Gene expression analysis of STAT5‐induced senescence revealed changes in the expression of genes coding for cytokines, proteins in cytokine signaling pathways, and several metabolic enzymes. We discuss a model called senescence‐induced senescence, in which cytokines secreted by senescent cells can propagate the process as a function of age.

Senescence

STAT5

10.1111/j.1749-6632.2010.05192.x

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Supplementary Figures S1-S7 from A CDK4/6-Dependent Epigenetic Mechanism Protects Cancer Cells from PML-induced Senescence

Mariana Acevedo Mathieu Vernier Lian Mignacca Frédéric Lessard Geneviève Huot

<p>Disabling RB bypasses PML-induced senescence in normal human fibroblasts (S1); Cyclin-dependent kinase inhibitors p21 and p16INK4A cooperate with PML to inhibit cancer cell proliferation (S2); CDK inhibitors enhance PML-mediated growth arrest and senescence in tumor cell lines (S3); Gene Set Enrichment Analysis (GSEA) showing homology to our gene expression profiling (S4); Gene Set Enrichment Analysis (GSEA) showing homology to our gene expression profiling (S5); Palbociclib or 5-Aza-dC sensitise cells to PML-induced irreversible growth arrest (S6); palbociclib decreased DNMT1 levels in a dose dependent manner (S7).</p>

Palbociclib

Senescence

Cyclin-dependent kinase 4

10.1158/0008-5472.22409094.v1

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