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Mitochondrial BCRP sustains the proliferation and survival of drug-resistant breast-cancer cells by regulating intracellular ROS

ABSTRACT: Mitochondrial BCRP sustains the proliferation and survival of drug-resistant breast-cancer cells by regulating intracellular ROS

PROVIDER: PRJNA752771 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15365849_1.fastq.gz	Fastqsanger.gz
	SRR15365849_2.fastq.gz	Fastqsanger.gz
	SRR15365850_1.fastq.gz	Fastqsanger.gz
	SRR15365850_2.fastq.gz	Fastqsanger.gz
	SRR15365851_1.fastq.gz	Fastqsanger.gz

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Mitochondrial BCRP sustains the proliferation and survival of drug-resistant breast-cancer cells by regulating intracellular ROS

Project description:ATP-binding cassette (ABC) transporter family are major contributors to the drug-resistance establishment of breast cancer cells. Breast cancer resistant protein (BCRP), one of the ABC transporters, has long been recognized as a pump that effluxes the therapeutic drugs against the concentration gradient. However, recent studies suggest that the biological function of BCRP is not limited in its drug-pump activity. Herein, the role of BCRP in the proliferation and survival of drug-resistant breast cancer cells was investigated. We found that BCRP is not the major drug pump to efflux epirubicin in the resistant cells that express multiple ABC transporters. Silencing of BCRP significantly impairs cell proliferation and induces apoptosis of the resistant cells in vitro and in vivo. RNA-sequencing and high-throughput proteomics suggest that BCRP is an inhibitory factor of oxidative phosphorylation (OXPHOS). Further research suggests that BCRP is localized in the mitochondria of the resistant cells. Knockdown of BCRP elevated the intracellular reactive oxygen species (ROS) level and eventually promotes the cell to undergo apoptosis. This study demonstrated that BCRP exerts important onco-promoting functions in the drug-resistant breast cancer cells independent of its well-recognized drug-efflux activity, which shed new light on understanding the complex functional role of ABC transporters in drug-resistant cells.

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Mitochondrial Breast Cancer Resistant Protein Sustains the Proliferation and Survival of Drug-Resistant Breast Cancer Cells by Regulating Intracellular Reactive Oxygen Species.

Project description:ATP-binding cassette (ABC) transporter family are major contributors to the drug resistance establishment of breast cancer cells. Breast cancer resistant protein (BCRP), one of the ABC transporters, has long been recognized as a pump that effluxes the therapeutic drugs against the concentration gradient. However, recent studies suggest that the biological function of BCRP is not limited in its drug pump activity. Herein, the role of BCRP in the proliferation and survival of drug-resistant breast cancer cells was investigated. We found that BCRP is not the major drug pump to efflux epirubicin in the resistant cells that express multiple ABC transporters. Silencing of BCRP significantly impairs cell proliferation and induces apoptosis of the resistant cells in vitro and in vivo. RNA-sequencing and high-throughput proteomics suggest that BCRP is an inhibitory factor of oxidative phosphorylation (OXPHOS). Further research suggests that BCRP is localized in the mitochondria of the resistant cells. Knockdown of BCRP elevated the intracellular reactive oxygen species level and eventually promotes the cell to undergo apoptosis. This study demonstrated that BCRP exerts important onco-promoting functions in the drug-resistant breast cancer cells independent of its well-recognized drug efflux activity, which shed new light on understanding the complex functional role of ABC transporters in drug-resistant cells.

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Project description:Disruption of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how nearly lethal stresses affect circadian clocks. We found that near-lethal doses of reactive oxygen species (ROS)-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) M-bM-^@M-^Smediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-orchestrated crosstalk between the circadian, HSR, NFM-NM-:B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in ROS-inducible disorders, various diseases, and death. Gene expression was measured 4h, 20h and 32h after treatment with 5 mM H2O2 for 10 min.

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ROS control in human iPS cells reveals early events in spontaneous carcinogenesis

Project description:We developed a system to control the intracellular level of reactive oxygen species (ROS) in human iPS cells. By introducing a specific substitution (I69E) into the SDHC protein, a component of the mitochondrial respiratory chain complex, the intracellular ROS level considerably increased. This caused an abnormal development of iPS cells, and these abnormalities were reverted by the overproduction of mitochondria-targeted catalase. When ROS-overproducing iPS cells (ChiPSC12-M cells) were used for subcutaneous inoculation on the backs of nude mice, the mice exhibited tumor formation. The expression of tumor-related FOXC1 transcription factor increased as early as 4 h after the the development of ROS-overproducing iPS cells was initiated. An RNA-seq analysis revealed that 27 transcript clusters among the more than 20,000 transcrips that were examined were highly expressed at 4 h after the initiation of tumor development in ChiPSC12-M cells. Some of these overexpressed transcripts might make networks to activate protooncogenes for spontaneous carcinogenesis.

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