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Siberchicot, C.

Publications and source records attributed to Siberchicot, C..

5 recordsLinked to original sources

Direct effects on gene transcription revealed by global and CRISPR-targeted oxidative DNA damage

Oxidative stress induces rapid expression changes of specific genes. However, whether these changes are due to direct and local DNA oxidation and whether they depend on the repair machinery is still debated. Here, we show by total RNA-Seq that upon oxidative stress, many genes are either rapidly repressed or activated. The early transcriptional response also includes the activation of many read-through RNAs. Importantly, degradation of the endogenous OGG1 DNA glycosylase showed that the early repression of these genes partially depends on OGG1, therefore demonstrating that these genome expression changes are due to the processing of oxidized DNA. We further demonstrate by ChIPseq against total or S5-phosphorylated RNA polymerase II that transcriptional regulation by oxidative stress involves changes in the recruitment of RNA polymerase II to transcription start sites. Finally, through the use of a chemoptogenetic system allowing the targeting of ROS to chosen genomic loci, we were able to reproduce repression of some genes through the local induction of oxidative DNA damage at their promoters, demonstrating that local DNA oxidation directly affects transcription of genes. Altogether, our results show that local oxidative DNA damage leads to alterations in the activity of specific promoters by a mechanism dependent on repair processes.

genomics↗

G-quadruplex ligand RHPS4 compromises cellular radio-resistance by blocking the increase in mitochondrial mass and activity induced by ionising irradiation.

A major challenge in radiotherapy is to enhance tumor cell sensitivity to radiation while minimizing damage to healthy tissues. Ionising radiation (IR) induces mitochondrial DNA (mtDNA) alterations that can impair mitochondrial function and cell survival. Since mitochondria play a key role in tumor cell proliferation, they represent a promising therapeutic target for cancer treatment. In this study, we characterized the impact of different IR sources on mitochondrial function in radioresistant cancer cells. Our findings revealed several adaptive responses that may contribute to radioresistance, including increased mtDNA content, mitochondrial mass, enhanced activity, and hyperfusion of the mitochondrial network. Notably, the use of mitochondrial-targeted G-quadruplex (G4) ligands, which block mtDNA replication and transcription, disrupted these responses, reducing cancer cell survival in an mtDNA-dependent manner. These results demonstrate that mitochondrial adaptations contribute to radioresistance and highlight mitochondria as a novel target for the radiosensitizing effects of G4-ligands, extending their potential beyond telomere destabilization.

cell biology↗

Identification of key residues of the DNA glycosylase OGG1 controlling efficient DNA scanning and recruitment to oxidized bases in living cells

The DNA-glycosylase OGG1 oversees the detection and clearance of the 7,8-dihydro-8-oxoguanine (8-oxoG), which is the most frequent form of oxidized base in the genome. This lesion is deeply buried within the double-helix and its detection requires careful inspection of the bases by OGG1 via a mechanism that remains only partially understood. By analyzing OGG1 dynamics in the nucleus of living human cells, we demonstrate that the glycosylase constantly scans the DNA by rapidly alternating between diffusion within the nucleoplasm and short transits on the DNA. This scanning process, that we find to be tightly regulated by the conserved residue G245, is crucial for the rapid recruitment of OGG1 at oxidative lesions induced by laser micro-irradiation. Furthermore, we show that residues Y203, N149 and N150, while being all involved in early stages of 8-oxoG probing by OGG1 based on previous structural data, differentially regulate the scanning of the DNA and recruitment to oxidative lesions.

cell biology↗

Loss of CD24 promotes radiation- and chemo-resistance by inducing stemness properties associated with a hybrid E/M state in breast cancer cells

There is compelling evidence that cancer stem cells (CSCs) play an essential role in failure of conventional antitumor therapy. In breast cancer, CD24-/low/CD44+ phenotype as well as a high aldehyde dehydrogenase activity (ALDH+) are widely associated with CSC subtypes. Furthermore, CD24-/low/CD44+ pattern is also characteristic of the mesenchymal cells generated by an epithelial-mesenchymal transition (EMT). CD24 is a surface marker expressed in many tumor types, however, its biological functions and role in cancer progression and treatment resistance remain poorly documented. We have previously shown that loss of CD24 expression in breast cancer cells is associated with radiation resistance, in relationship with the control of oxidative stress. Because ROS are known to mediate the effects of anticancer drugs as well as ionizing radiation, we investigated if CD24 could be defined as an actor of both radiation- and chemo-resistance of breast cancer cells. Using the HMLE breast cancer cell model, we observed that loss of CD24 expression induces stemness properties associated with the acquisition of a hybrid E/M phenotype. The CD24-/low cells were intrinsically more resistant than CD24+ cells. The resistance was linked to a lower level of ROS, and CD24 controlled ROS levels through the regulation of mitochondrial functions independently of antioxidant activity. Together, these results suggest a key role of CD24 in de-differentiation process of breast cancer cells, promoting acquisition of therapeutic resistance properties.

cancer biology↗

An adaptive pre-DNA-damage-response protects genome integrity

The DNA damage response (DDR) interrupts cell cycle progression to restore genome integrity. However, unchallenged proliferating cells are continually exposed to endogenous stress, raising the question of a stress-threshold for DDR activation. Here, we identified a stress threshold below which primary human fibroblasts, activate a cell-autonomous response that not activates full DDR and not arrests cell cycle progression. We characterized this "pre-DDR" response showing that it triggers the production of reactive oxygen species (ROS) by the NADPH oxidases DUOX1 and DUOX2, under the control of NF-{kappa}B and PARP1. Then, replication stress-induced ROS (RIR) activates the FOXO1 detoxifying pathway, preventing the nuclear accumulation of the pre-mutagenic 8-oxoGuanine lesion, upon endogenous as well as exogenous pro-oxidant stress. Increasing the replication stress severity above the threshold triggers the canonical DDR, leading to cell cycle progression arrest, but also to RIR suppression. These data reveal that cells adapt their response to stress severity, unveiling a tightly regulated "pre-DDR" adaptive response that protects genome integrity without arresting cell cycle progression.

cell biology↗