IκB Cancer Research Results

IκB, IκB kinase(α): Click to Expand ⟱
Source:
Type:
IκB (Inhibitor of Nuclear Factor kappa B) proteins are critical regulators of the NF-κB signaling pathway, which plays a significant role in inflammation, immune response, and cell survival.
IκB kinase/NF-κB (IKK/NF-κB) signaling pathways play critical roles in a variety of physiological and pathological processes. One function of NF-κB is promotion of cell survival through induction of target genes, whose products inhibit components of the apoptotic machinery in normal and cancerous cells.
NFKB inhibitor α (IκB‑α) acts as a negative regulator of the classical NF‑κB pathway through its ability to maintain the presence of NF‑κB in the cytoplasm.
IκB (Inhibitor of κB) proteins play a crucial role in regulating the NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) signaling pathway, which is involved in various cellular processes, including inflammation, immune response, and cell survival. The NF-κB pathway is tightly regulated, and its dysregulation has been implicated in the development and progression of various cancers.
In many cancers, the degradation of IκB is enhanced, leading to constitutive activation of NF-κB. This can promote tumor growth and survival by upregulating genes involved in cell proliferation and anti-apoptotic factors.

IκB proteins generally act as tumor suppressors by inhibiting NF-κB activity. When IκB is downregulated, NF-κB is activated, leading to increased cell proliferation, survival, and inflammation, which can promote tumor growth.

It is generally down regulated in cancers, with poorer prognosis.
Scientific Papers found: Click to Expand⟱
1074- ART/DHA,    Artemisinin attenuates lipopolysaccharide-stimulated proinflammatory responses by inhibiting NF-κB pathway in microglia cells
- in-vitro, Nor, BV2
*TNF-α↓,
*IL6↓,
*MCP1↓,
*NO↓,
*iNOS↓,
*IκB↑,

1532- Ba,    Baicalein as Promising Anticancer Agent: A Comprehensive Analysis on Molecular Mechanisms and Therapeutic Perspectives
- Review, NA, NA
ROS↑, Baicalein initially incited the formation of ROS, which subsequently aimed at endoplasmic reticulum stress and stimulated the Ca2+/-reliant mitochondrial death pathway.
ER Stress↑,
Ca+2↑,
MMPs↓,
Cyt‑c↑, cytochrome C release
Casp3↑,
ROS↑, Baicalein on apoptosis in human bladder cancer 5637 cells was investigated, and it was found that it induces ROS generation
DR5↑, Baicalein activates DR5 up-regulation
ROS↑, MCF-7 cells by inducing mitochondrial apoptotic cell death. It does this by producing ROS, such as hydroxyl radicals, and reducing Cu (II) to Cu (I) in the Baicalein–Cu (II) system
BAX↑,
Bcl-2↓,
MMP↓,
Casp3↑,
Casp9↑,
P53↑,
p16↑,
P21↑,
p27↑,
HDAC10↑, modulating the up-regulation of miR-3178 and Histone deacetylase 10 (HDAC10), which accelerates apoptotic cell death
MDM2↓, MDM2-mediated breakdown
Apoptosis↑,
PI3K↓, baicalein-influenced apoptosis is controlled via suppression of the PI3K/AKT axis
Akt↓,
p‑Akt↓, by reducing the concentrations of p-Akt, p-mTOR, NF-κB, and p-IκB while increasing IκB expression
p‑mTOR↓,
NF-kB↓,
p‑IκB↓,
IκB↑,
BAX↑,
Bcl-2↓,
ROS⇅, Based on its metabolic activities and intensity, Baicalein can act as an antioxidant and pro-oxidant.
BNIP3↑, Baicalein also increases the production of BNIP3 which is a protein stimulated by ROS and promotes apoptosis
p38↑,
12LOX↓, inhibition of 12-LOX (Platelet-type 12-Lipoxygenase)
Mcl-1↓,
Wnt?, decreasing Wnt activity
GLI2↓, Baicalein significantly reduced the presence of Gli-2, a crucial transcription factor in the SHH pathway
AR↓, downregulating the androgen receptor (AR)
eff↑, PTX/BAI NE could increase intracellular ROS levels, reduce cellular glutathione (GSH) levels, and trigger caspase-3 dynamism in MCF-7/Tax cells. Moreover, it exhibited higher efficacy in inhibiting tumors in vivo

1263- CAP,    Capsaicin inhibits the migration and invasion via the AMPK/NF-κB signaling pathway in esophagus sequamous cell carcinoma by decreasing matrix metalloproteinase-9 expression
- in-vitro, ESCC, Eca109
TumCMig↓,
TumCI↓,
MMP9↓,
p‑AMPK↑,
SIRT1↑,
NF-kB↓, capsaicin retrains the invasion and migration of Eca109 cells by inhibiting NF-κB p65 via the AMPK-SIRT1 and the AMPK-IκBa signaling pathways, which cause MMP-9 expression inhibition.
p‑IκB↑,

1503- EGCG,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
selectivity↑, EGCG has been shown to induce apoptosis and cell cycle arrest in many cancer cells without affecting normal cells
DNMT1↓, inhibition of DNMT1 leading to demethylation and reactivation of methylation-silenced genes.
RECK↑, EGCG-induced epigenetic reactivation of RECK
MMPs↓, negatively regulates matrix metalloproteinases (MMPs)
TumCI↓, inhibits tumor invasion, angiogenesis, and metastasis
angioG↓,
TumMeta↓,
HATs↓, EGCG has strong HAT inhibitory activity
IκB↑, increases the level of cytosolic IκBα
NF-kB↓, suppresses tumor necrosis factor α-induced NF-κB activation
IL6↓,
COX2↓,
NOS2↓,
ac‑H3↑, increased the levels of acetylated histone H3 (LysH9/18) and H4 levels
ac‑H4↑,
eff↑, EGCG may synergize with the HDAC inhibitory action of vorinostat to help de-repress silenced tumor suppressor genes regulating key functions such as proliferation and cell survival

1003- SSE,    Sodium selenite inhibits proliferation of lung cancer cells by inhibiting NF-κB nuclear translocation and down-regulating PDK1 expression which is a key enzyme in energy metabolism expression
- vitro+vivo, Lung, NA
NF-kB↓,
PDK1↓,
p‑p65↑,
p‑IκB↑,
BAX↑,
lactateProd↓,
MMP↓,
Cyt‑c↑, release of Cytochrome C
mitResp↑,
Apoptosis↑,

2132- TQ,    Thymoquinone treatment modulates the Nrf2/HO-1 signaling pathway and abrogates the inflammatory response in an animal model of lung fibrosis
- in-vivo, Nor, NA
*Weight∅, BM administration resulted in a significant weight loss, which was ameliorated by TQ treatment.
*antiOx↑, BMILF was associated with a reduction in the antioxidant mechanisms and increased lipid peroxidation (abnormalities were diminished with TQ treatment)
*lipid-P↓,
*MMP7↓, elevated levels of inflammatory cytokines, MMP-7 expression, apoptotic markers (caspase 3, Bax, and Bcl-2), and fibrotic changes including TGF-β and hydroxyproline levels in lung tissues were evident. These abnormalities were diminished with TQ
*Casp3↓,
*BAX↓,
*TGF-β↓,
*Diff↑, differential cell count in BALF was significantly improved in rats treated with TQ
*NRF2↓, TQ also produced a dose-dependent reduction in the expressions of Nrf2, Ho-1 and TGF-β. (ai:once TQ reduces oxidative damage, the demand for high Nrf2 activity drops)
*HO-1↓,
*NF-kB↓, NF-jB protein expression has been significantly and dose dependently decreased in TQ treated groups (10 and 20 mg/kg bw)
*IκB↑, IkBa has been significantly and dose dependently increase in TQ treated groups (10 and 20 mg/kg bw).


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 3,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

mitResp↑, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   p‑AMPK↑, 1,   lactateProd↓, 1,   PDK1↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 3,   Bcl-2↓, 2,   Casp3↑, 2,   Casp9↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   Mcl-1↓, 1,   MDM2↓, 1,   p27↑, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   HATs↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   p16↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC10↑, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   Wnt?, 1,  

Migration ⓘ

Ca+2↑, 1,   GLI2↓, 1,   MMP9↓, 1,   MMPs↓, 2,   RECK↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IκB↑, 2,   p‑IκB↓, 1,   p‑IκB↑, 2,   NF-kB↓, 4,   p‑p65↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   IL6↓, 1,   NOS2↓, 1,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   HO-1↓, 1,   lipid-P↓, 1,   NRF2↓, 1,  

Cell Death ⓘ

BAX↓, 1,   Casp3↓, 1,   iNOS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,  

Migration ⓘ

MMP7↓, 1,   TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   IκB↑, 2,   MCP1↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

Weight∅, 1,  
Total Targets: 18

Scientific Paper Hit Count for: IκB, IκB kinase(α)
1 Artemisinin
1 Baicalein
1 Capsaicin
1 EGCG (Epigallocatechin Gallate)
1 Selenite (Sodium)
1 Thymoquinone
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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