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The anticancer Ruthenium drug BOLD-100 regulates apoptosis of BRAFMT colorectal cancer cells through modulation of the AhR/ROS/ATR signalling axis.

ABSTRACT: The anticancer Ruthenium drug BOLD-100 regulates apoptosis of BRAFMT colorectal cancer cells through modulation of the AhR/ROS/ATR signalling axis.

PROVIDER: PRJNA1062832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27474455_1.fastq.gz	Fastqsanger.gz
	SRR27474455_2.fastq.gz	Fastqsanger.gz
	SRR27474456_1.fastq.gz	Fastqsanger.gz
	SRR27474456_2.fastq.gz	Fastqsanger.gz
	SRR27474457_1.fastq.gz	Fastqsanger.gz

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The anticancer Ruthenium drug BOLD-100 regulates apoptosis of BRAFMT colorectal cancer cells through modulation of the AhR/ROS/ATR signalling axis.

Project description:The understanding of how oncogenes modulate the mechansim of action of compounds relies on interrogating acute and longer transcriptional changes following treatment. We report here the transcriptional profiles of an isogenic cell line model VACO432 (BRAFMT V600E/WT) and VT1 (BRAFWT/-) following 3H and 24H treatment with a novel ruthenium compound BOLD-100. We compare the two cell line models based on their BRAF status to identify transcriptional changes modulted by oncogenic BRAF.

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Interaction with ribosomal proteins accompanies ER stress-induction of the anticancer metallodrug BOLD-100/KP1339

Project description:The ruthenium-based anticancer agent BOLD-100/KP1339 has shown promising results in several in vitro and in vivo tumour models, as well as in early clinical trials. However, its mode of action remains to be fully elucidated. Recent evidence identified ER stress-induction and concomitant down-modulation of HSPA5 (GRP78) as key drug effects. By exploiting the naturally formed adduct between BOLD-100 and human serum albumin as an immobilization strategy, we were able to perform target profiling experiments that revealed the ribosomal proteins RPL10, RPL24 and the transcription factor GTF2I as potential interactors of this ruthenium(III) anticancer agent. Integrating these findings with proteomic profiling and transcriptomic experiments supported ribosomal disturbance and concomitant induction of endoplasmic reticulum (ER) stress. The formation of poly-ribosomes and ER swelling of treated cancer cells by electron microscopy validated this finding. Thus, the direct interaction of BOLD-100 with ribosomal proteins seems to accompany ER stress-induction and modulation of GRP78 in cancer cells.

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Hyperosmotic stress induces 2-cell-like cells through ROS and ATR signaling

Project description:Mouse embryonic stem cells (ESCs) display pluripotency features characteristic of the inner cell mass of the blastocyst. ESC cultures are highly heterogeneous and include a rare population of cells, which recapitulate characteristics of the 2-cell embryo, referred to as 2-cell-like cells (2CLCs). Whether and how ESC and 2CLC respond to environmental cues has not been fully elucidated. Here, we investigate the impact of mechanical stress on the reprogramming of ESC to 2CLC. We show that hyperosmotic stress induces 2CLC and that this induction can occur even after a recovery time from hyperosmotic stress, suggesting a memory response. Hyperosmotic stress in ESCs leads to accumulation of reactive-oxygen species (ROS) as well as ATR checkpoint activation. Importantly, preventing either elevated ROS levels or ATR activation impairs hyperosmotic-mediated 2CLC induction. We further show that ROS generation and the ATR checkpoint act within the same molecular pathway in response to hyperosmotic stress to induce 2CLCs. Altogether, these results shed light on the response of ESC to mechanical stress and on our understanding of 2CLC reprogramming.

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