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Regulation of pyroptosis in radiation induces mouse intestine cells

ABSTRACT: Regulation of pyroptosis in radiation induces mouse intestine cells

PROVIDER: PRJNA871879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21151512_1.fastq.gz	Fastqsanger.gz
	SRR21151513_1.fastq.gz	Fastqsanger.gz
	SRR21151514_1.fastq.gz	Fastqsanger.gz
	SRR21151515_1.fastq.gz	Fastqsanger.gz
	SRR21151516_1.fastq.gz	Fastqsanger.gz

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Regulation of pyroptosis in radiation induces mouse intestine cells

Project description:Pyroptosis is a recently discovered form of lytic cell death that is characterized by cell swelling and formation of pores and large bubbles on the plasma membrane. We find radiation could induce pyroptosis in human colorectal cancer HCT116 cells, and irradiation induces pyroptosis in mouse normal intestine MODEK cells only after 36 hours and over 8.0 Gy. In view of the significant pyroptosis effect of MODE-K cells, we selected 4Gy and 12Gy, 24h and 48h for experiments. After ONT full-length transcriptome sequencing, the cell pyroptosis model can screen out the differential genes related to cell pyroptosis, which is helpful to further explore the mechanism of pyroptosis of MODE-K cells.

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Project description:summary (1)Objective: To investigate the antileukemic role of Lip-1 in K562 leukemia cells. (2)Methods: We performed CCK-8, flow cytometry, microscopy, western blotting assay, next generation sequencing, PCR assays to evaluate the effect of Lip-1 in K562 leukemia cells. (3)Results: Lip-1 inhibited K562 cell proliferation in a dose- and time-dependent manner. RNA sequencing revealed several pathways that were affected by Lip-1, such as the G1/S transition of the mitotic cell cycle and extrinsic or intrinsic apoptotic signaling pathways. The results of flow cytometry indicated that Lip-1 arrests the cell cycle. K562 cells were characterized by swelling and plasma membrane rupture. The expression of the hallmark of pyroptosis, the cleaved N-terminal GSDME, increased. Endoplasmic reticulum stress and autophagy were involved in Lip-1-induced cell death. (4)Conclusion：Lip-1 induces cell cycle arrest, apoptosis, and secondary pyroptosis in K562 leukemia cells, which provides new hope for the treatment of leukemia.

2022-05-31 | GSE205036 | GEO

Citric acid, an ovarian cancer metabolite, induces pyroptosis via caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer

Project description:Malignant tumors display profound changes in cellular metabolism, yet how these altered metabolites affect the development and growth of tumors is not fully understood. Here, we used metabolomics to analyze the metabolic profile differences in ovarian cancer, and found that citric acid (CA) is the most significantly downregulated metabolite. Recently, CA has been reported to inhibit the growth of a variety of tumor cells, but whether it is involved in pyroptosis of ovarian cancer and its potential molecular mechanisms still remains to be further investigated. Here, we demonstrated that CA inhibits the growth of ovarian cancer cells in a dose-dependent manner. RNA-seq analysis revealed that CA significantly promoted the expression of thioredoxin interacting protein (TXNIP) and caspase-4 (CASP4). Morphologic examination by transmission electron microscopy indicated that CA-treated ovarian cancer cells exhibited typical pyroptosis characteristics. Further mechanistic analyses showed that CA facilitates pyroptosis via CASP4/TXNIP-NLRP3-Gesdermin-d (GSDMD) pathway in ovarian cancer. This study elucidated that CA induces ovarian cancer cell death through classical and non-classical pyroptosis pathways, which may be beneficial as an ovarian cancer therapy.

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