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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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
The heterodimer of NF-κB...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

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
The heterodimer of NF-κB...
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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Updated: May 14, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
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Published on: January 18, 2017

Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.

Elżbieta Mitka-Krysiak1, Katarzyna Król-Jatręga1, Piotr Ossowski1

  • 1Collegium Medicum, WSB University, 41-300 Dabrowa Gornicza, Poland.

International Journal of Molecular Sciences
|May 13, 2026
PubMed
Summary

Nuclear factor kappa B (NF-κB) signaling is activated across all breast cancer subtypes in Polish women, driving tumor growth. Specific microRNAs (miRNAs) are dysregulated, potentially contributing to this activation and offering therapeutic targets.

Keywords:
breast cancermicro RNA (miRNA)nuclear factor kappa B (NF-κB) signaling

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Published on: November 2, 2018

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Nuclear factor kappa B (NF-κB) signaling is crucial in inflammation, immunity, cell survival, and cancer progression.
  • Constitutive NF-κB activation is common in breast cancer, promoting tumor growth, treatment resistance, and metastasis.
  • MicroRNAs (miRNAs) are key gene expression regulators that can modulate NF-κB signaling.

Purpose of the Study:

  • To identify miRNAs regulating NF-κB signaling genes across five molecular subtypes of breast cancer in Polish women.
  • To investigate the role of miRNA dysregulation in NF-κB pathway activation in breast cancer.
  • To explore potential miRNA-based therapeutic strategies for breast cancer.

Main Methods:

  • Analysis of tumor and normal tissue samples from 405 breast cancer patients across five subtypes.
  • Gene expression profiling using mRNA microarrays and RT-qPCR for NF-κB-related genes.
  • Protein level assessment via ELISA and miRNA profiling using miRNA microarrays; validation with miRDB database.

Main Results:

  • Consistent upregulation of key NF-κB signaling genes (MAP3K7, TAB2, TNFAIP3, CSNK2A1, BCL2L1, XIAP, CXCL2, PLAU) observed across all breast cancer subtypes.
  • Downregulation of specific miRNAs (miR-1297, miR-30a, miR-134, miR-125b, miR-4329) identified as potential regulators of upregulated genes.
  • Evidence of a subtype-independent activation of the canonical NF-κB pathway, with dysregulated miRNAs contributing to altered gene expression.

Conclusions:

  • A common NF-κB-driven oncogenic program exists across molecular subtypes of breast cancer.
  • Specific miRNA dysregulation contributes to the activation of canonical NF-κB signaling in breast cancer.
  • Findings suggest potential for miRNA-based therapeutic strategies targeting inflammation, survival, and treatment resistance in breast cancer.