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Parthenolide induces ROS-dependent cell death in human gastric cancer cells

ABSTRACT: Parthenolide induces ROS-dependent cell death in human gastric cancer cells

PROVIDER: PRJNA899475 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22228133_1.fastq.gz	Fastqsanger.gz
	SRR22228133_2.fastq.gz	Fastqsanger.gz
	SRR22228134_1.fastq.gz	Fastqsanger.gz
	SRR22228134_2.fastq.gz	Fastqsanger.gz
	SRR22228135_1.fastq.gz	Fastqsanger.gz

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Parthenolide induces ROS-dependent cell death in human gastric cancer cells

Project description:Parthenolide (PN), a key active ingredient of feverfew, has been used to treat gastrointestinal disorders. However, the mechanism of the cytotoxic effect exerted by PN on tumor cells is not elucidated now. MGC-803 cells treated with and without PN were separately subjected to high throughput RNA sequencing (RNA-Seq).

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Project description:Reactive oxygen species (ROS) play a vital role in conveying the cytotoxicity and resistance of most chemo-drugs. Thus, a better understanding of the detailed activities against oxidative stress in cancer cells may provide novel insights into the discovery of common mechanisms underlying chemoresistance. In this study, taking advantage of a customized screening strategy based on transcriptome sequencing (RNA-Seq) technology, we identified a novel lncRNA, designated FUAT1, as a key non-genetic player that participates in ROS-mediated intrinsic chemoresistance in gastric cancer (GC) cells. The role of the FUAT1 regulatory axis in chemoresistance was further explored by using a series of in vitro and in vivo assays, including gain/loss-of-function and rescue experiments. Mechanistically, FUAT1 could upregulate TNS4 by sponging miR-140-5p, allowing GC cells to survive upon chemotherapy via inhibition of ROS-mediated apoptosis. Clinically, the FUAT1/TNS4 regulatory axis is negatively associated with overall and progression-free survival in gastric and colon cancer patients treated with 5-FU adjuvant chemotherapy. Our findings touch on a fundamental adaptive mechanism for the survival of cancer cells upon chemotherapy, providing a novel insight into the development of strategies to overcome chemoresistance.

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Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells.

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Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-Seq]

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

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