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Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [DH]

ABSTRACT: Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [DH]

PROVIDER: PRJNA616418 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11453510.fastq.gz	Fastqsanger.gz
	SRR11453511.fastq.gz	Fastqsanger.gz
	SRR11453512.fastq.gz	Fastqsanger.gz
	SRR11453513.fastq.gz	Fastqsanger.gz
	SRR11453514.fastq.gz	Fastqsanger.gz

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Protein Kinase / suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [DH]

Project description:Oxidative stress plays a critical role in liver tissue damage and in hepatocellular carcinoma (HCC) initiation and progression. However, the mechanisms that regulate autophagy and metabolic reprogramming during the generation of reactive oxygen species (ROS), and how ROS promotes tumorigenesis, still need to be fully understood. We show that protein kinase C (PKC) / loss in hepatocytes promotes autophagy and oxidative phosphorylation. This results in ROS generation, which through NRF2 drives HCC cell autonomously and non-autonomously. Although PKC / promotes tumorigenesis in oncogene-driven cancer models, emerging evidence demonstrate that it is a tumor suppressor in more complex carcinogenic processes. Consistently, PKC / levels negatively correlate with HCC histological tumor grade, establishing this kinase as a tumor suppressor in liver cancer.

2020-06-30 | GSE147800 | GEO

Protein Kinase / suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [RD]

Project description:Oxidative stress plays a critical role in liver tissue damage and in hepatocellular carcinoma (HCC) initiation and progression. However, the mechanisms that regulate autophagy and metabolic reprogramming during the generation of reactive oxygen species (ROS), and how ROS promotes tumorigenesis, still need to be fully understood. We show that protein kinase C (PKC) / loss in hepatocytes promotes autophagy and oxidative phosphorylation. This results in ROS generation, which through NRF2 drives HCC cell autonomously and non-autonomously. Although PKC/ promotes tumorigenesis in oncogene-driven cancer models, emerging evidence demonstrate that it is a tumor suppressor in more complex carcinogenic processes. Consistently, PKC / levels negatively correlate with HCC histological tumor grade, establishing this kinase as a tumor suppressor in liver cancer.

2020-06-30 | GSE147778 | GEO

Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes.

Project description:Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes.

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Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [RD]

Project description:Protein Kinase 휆/휄 suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes [RD]

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Protein Kinase / suppresses liver cancer by repressing autophagy and oxidative phosphorylation in hepatocytes.

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-30 | GSE147801 | GEO

Translational control of autophagy by Orb in the Drosophila germline [mature]

Project description:Drosophila Orb, the homologue of vertebrate CPEB is a key translational regulator involved in oocyte polarity and maturation through poly(A) tail elongation of specific mRNAs. orb has also an essential function during early oogenesis which has not been addressed at the molecular level. Here, we show that orb prevents cell death during early oogenesis, thus allowing oogenesis to progress. It does so through the repression of autophagy, by directly repressing, together with the CCR4 deadenylase, the translation of Autophagy-specific gene 12 (Atg12) mRNA. Autophagy and cell death observed in orb mutant ovaries are reduced by decreasing Atg12 or other Atg mRNA levels. These results reveal a role of Orb in translational repression and identify autophagy as an essential pathway regulated by Orb during early oogenesis. Importantly, they also establish translational regulation as a major mode of control of autophagy, a key process in cell homeostasis in response to environmental cues. Orb RIP-chip vs mock IP on ovaries from mature 3-5 day old females.

2016-07-03 | E-GEOD-74475 | biostudies-arrayexpress

Translational control of autophagy by Orb in the Drosophila germline [early]

2016-07-03 | E-GEOD-74474 | biostudies-arrayexpress

Sphingomonas aliaeris strain:DH-S5 | isolate:DH-S5

Project description:Sphingomonas aliaeris strain:DH-S5 | isolate:DH-S5 Genome sequencing

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Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

Project description:Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes via Foxk-Sin3-mediated transcriptional control. Examination of (1) chromatin binding of Foxk1 and Sin3A in non-starved myoblasts and (2) gene expression profiling upon either starvation or siRNA-mediated depletion of Foxk1 relative to a non-starved control.

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