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NF-κB controls energy homeostasis and metabolic adaptation by upregulating mitochondrial respiration.

TLDR
It is reported that NF-κB organizes energy metabolism networks by controlling the balance between the utilization of glycolysis and mitochondrial respiration and establishes a role for NF-B in metabolic adaptation in normal cells and cancer.
Abstract
Franzoso and colleagues show that NF-κB protects cells from nutrient-starvation-induced necrosis by upregulating mitochondrial respiration through increased p53-dependent expression of the SCO2 enzyme. Conversely, inhibition of NF-κB results in increased aerobic glycolysis, known as the Warburg effect, thus promoting oncogenic transformation, and affects metabolic adaptation during tumorigenesis in vivo.

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NF-κB, inflammation, immunity and cancer: coming of age

TL;DR: How the initial discovery of a role for NF-κB in linking inflammation and cancer led to an improved understanding of tumour-elicited inflammation and its effects on anticancer immunity is discussed.
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Reactive Oxygen Species in Metabolic and Inflammatory Signaling.

TL;DR: The role of ROS in the regulation metabolic/inflammatory diseases including atherosclerosis, diabetes mellitus, and stroke is highlighted and the balance ROS signaling plays in both physiology and pathophysiology is understood.
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Mitochondrial Dynamics and Metabolic Regulation.

TL;DR: The ways in which metabolic alterations convey changes in mitochondrial morphology and how disruption of mitochondrial morphology impacts cellular and organismal metabolism are reviewed.
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NF-κB, an Active Player in Human Cancers

TL;DR: Because of its vital role in various biologic activities, components of the NF-κB pathway need to be carefully selected and evaluated to design targeted therapies.
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The diverse and complex roles of NF-κB subunits in cancer

TL;DR: If the NF-κB pathway is to be properly exploited as a target for both anticancer and anti-inflammatory drugs, it is appropriate to reconsider the complex roles of the individual NF-σκB subunits.
References
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Journal ArticleDOI

Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation

TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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Self-eating and self-killing: crosstalk between autophagy and apoptosis

TL;DR: The functional relationship between apoptosis and autophagy is complex in the sense that, under certain circumstances,autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway.
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Nuclear factor-kappaB in cancer development and progression.

TL;DR: This article showed that NF-kappaB provides a mechanistic link between inflammation and cancer, and is a major factor controlling the ability of both pre-neoplastic and malignant cells to resist apoptosis-based tumour-surveillance mechanisms.
Journal ArticleDOI

A Third-Generation Lentivirus Vector with a Conditional Packaging System

TL;DR: It is demonstrated that the requirement for the tat gene can be offset by placing constitutive promoters upstream of the vector transcript, and the improved design presented here should facilitate testing of lentivirus vectors.
Journal ArticleDOI

Blinded by the Light: The Growing Complexity of p53

TL;DR: Control of p53's transcriptional activity is crucial for determining which p53 response is activated, a decision that must be understood if the next generation of drugs that selectively activate or inhibit p53 are to be exploited efficiently.
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