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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
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The Intrinsic Apoptotic Pathway01:31

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Receptor Downregulation in MVBs01:15

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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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NF-κB Signaling as a Central Driver of Cancer Cachexia.

Yan Li1, Hao Jiang2,3,4, Rui Chen5

  • 1Department of Cardiovascular Surgery, Southeast University Affiliated Nantong First People's Hospital, Nantong 226001, China.

Cancers
|February 27, 2026
PubMed
Summary

Nuclear factor kappa B (NF-κB) drives cancer cachexia by promoting inflammation and muscle wasting. Targeting NF-κB with various interventions shows promise in treating this complex metabolic syndrome.

Keywords:
NF-κB signalingadipose tissue remodelingcancer cachexiamuscle wastingsystemic inflammationtherapeutic targeting

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Area of Science:

  • Oncology
  • Metabolism
  • Molecular Biology

Background:

  • Cancer cachexia is a complex metabolic syndrome causing muscle wasting and inflammation.
  • The nuclear factor kappa B (NF-κB) signaling pathway is central to cachexia pathogenesis.
  • NF-κB dysregulates metabolism and promotes inflammation across multiple tissues.

Purpose of the Study:

  • To review the role of NF-κB in cancer cachexia.
  • To explore therapeutic strategies targeting NF-κB.
  • To highlight NF-κB as a translational target for cancer cachexia.

Main Methods:

  • Literature review integrating mechanistic insights and therapeutic advances.
  • Analysis of preclinical and clinical evidence on NF-κB inhibitors and anti-cachexia strategies.
  • Evaluation of multimodal treatment approaches.

Main Results:

  • Sustained NF-κB activation drives muscle proteolysis, inflammation, and metabolic dysfunction.
  • Pharmacologic inhibitors, anti-inflammatory drugs, and nutritional interventions show efficacy.
  • Multimodal therapies combining NF-κB modulation with other interventions yield synergistic benefits.

Conclusions:

  • NF-κB is a critical pathogenic axis in cancer cachexia.
  • Targeting NF-κB offers a promising therapeutic avenue.
  • Further translational research is warranted for effective cancer cachexia management.