IκB Cancer Research Results

IκB, IκB kinase(α): Click to Expand ⟱
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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⟱
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

160- CUR,    Curcumin inhibits prostate cancer metastasis in vivo by targeting the inflammatory cytokines CXCL1 and -2
- in-vitro, Pca, NA
CXCc↓, Curcumin downregulates the inflammatory cytokines CXCL1 and -2 in metastatic prostate cancer by targeting NFκB signaling
IκB↓,
NF-kB↓, The proinflammatory cytokines CXCL1/-2 act in a feedback loop reversely on the NFκB pathway
COX2↓,
SPARC↓,
EFEMP↓,
IKKα↓, We show that curcumin acts on the activation of NFκB through the stabilization of IκB in prostate cancer cells ju

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

1089- MAG,    Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways
- in-vitro, AML, RAW264.7
p‑IκB↓,
NF-kB↓,
p‑ERK↓,
p‑JNK↓,
p‑PI3K↓,
p‑Akt↓,
iNOS↓,
COX2↓,

204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

1746- RosA,    Rosmarinic acid sensitizes cell death through suppression of TNF-α-induced NF-κB activation and ROS generation in human leukemia U937 cells
- in-vitro, AML, U937
TNF-α↓, Rosmarinic acid (RA), a naturally occurring polyphenol flavonoid, has been reported to inhibit TNF-α-induced NF-κB activation in human dermal fibroblasts.
ROS↓, RA treatment significantly sensitizes TNF-α-induced apoptosis in human leukemia U937 cells through the suppression of nuclear transcription factor-kappaB (NF-κB) and reactive oxygen species (ROS).
Casp↑, Activation of caspases in response to TNF-α was markedly increased by RA treatment
NF-kB↓, RA also suppressed NF-κB activation through inhibition of phosphorylation and degradation of IκBα, and nuclear translocation of p50 and p65
IκB↓,
p50↓,
p65↓,
IAP1↓, This inhibition was correlated with suppression of NF-κB-dependent anti-apoptotic proteins (IAP-1, IAP-2, and XIAP)
IAP2↓,
XIAP↓,
Apoptosis↑, These results demonstrated that RA inhibits TNF-α-induced ROS generation and NF-κB activation, and enhances TNF-α-induced apoptosis.

1745- RosA,    Rosmarinic acid and its derivatives: Current insights on anticancer potential and other biomedical applications
- Review, Var, NA - Review, AD, NA
ChemoSideEff↓, updated review is to highlight the chemopreventive and chemotherapeutic effects of RA and its derivatives
ChemoSen↑,
antiOx↑, RA also showed antioxidant effects and suppressed the activity and expression of matrix metalloproteinase (MMP)− 2,9
MMP2↓,
MMP9↓,
p‑AMPK↑, show that RA prevents metastasis through AMPK phosphorylation and suppresses CRC cell growth
DNMTs↓, RA allegedly suppressed DNA methyltransferase activity in the human breast cancer MCF7 cell line
tumCV↓, A549 lung cancer cells were 50% suppressed by RA, which also prevented COX-2 activity in these cells.
COX2↓,
E-cadherin↑, upregulating E-cadherin expression while downregulating Vimentin and N-cadherin expression, indicating that RA could inhibit hepatocellular carcinoma cells' ability to invade by MMPs and EMT
Vim↓,
N-cadherin↓,
EMT↓,
Casp3↑, The activation of caspase-3 and caspase-9 by RA also prevented the migration and invasion of liver cancer cells
Casp9↓,
ROS↓, In addition to reducing ROS, RA also enhanced GSH synthesis, lowered the expression of MMP-2 and MMP-9
GSH↑,
ERK↓, By inhibiting ERK and Akt activation, RA may stop the progression of colon cancer
Akt↓,
ROS↓, In U937 cells, it has been demonstrated that treatment with RA in concentrations 60 µM suppresses ROS and NF-kB by blocking IκB-α from being phosphorylated and degraded and the nuclear translocation of p50 and p65
NF-kB↓,
p‑IκB↓,
p50↓,
p65↓,
neuroP↑, RA can prevent the pathophysiology of Alzheimer's disease by reducing Aβ aggregation
Dose↝, 60 µM suppresses ROS and NF-kB by blocking IκB-α from being phosphorylated and degraded and the nuclear translocation of p50 and p65

2084- TQ,    Thymoquinone, as an anticancer molecule: from basic research to clinical investigation
- Review, Var, NA
*ROS↓, An interesting study reported that thymoquinone is actually a potent apoptosis inducer in cancer cells, but it exerts antiapoptotic effect through attenuating oxidative stress in other types of cell injury
*chemoPv↑, antioxidant activity of thymoquinone is responsible for its chemopreventive activities
ROS↑, other studies reported thymoquinone induce apoptosis in cancer cells by exerting oxidative damage
ROS⇅, Another hypothesis states that thymoquinone acts as an antioxidant at lower concentrations and a prooxidant at higher concentrations
MUC4↓, Torres et al. [17] revealed that thymoquinone down-regulates glycoprotein mucin 4 (MUC4)
selectivity↑, thymoquinone was found to inhibit DNA synthesis, proliferation, and viability of cancerous cells, such as LNCaP, C4-B, DU145, and PC-3, but not noncancerous BPH-1 prostate epithelial cells [20].
AR↓, Down-regulation of androgen receptor (AR) and cell proliferation regulator E2F-1 was indicated as the mechanism behind thymoquinone’s action in prostate cancer
cycD1/CCND1↓, expression of STAT3-regulated gene products, such as cyclin D1, Bcl-2, Bcl-xL, survivin, Mcl-1 and vascular endothelial growth factor (VEGF), was inhibited by thymoquinone, which ultimately increased apoptosis and killed cancer cells
Bcl-2↓,
Bcl-xL↓,
survivin↓,
Mcl-1↓,
VEGF↓,
cl‑PARP↑, induction of the cleavage of poly-(ADP-ribose) polymerase (PARP
ROS↑, In ALL cell line CEM-ss, thymoquinone treatment generated reactive oxygen species (ROS) and HSP70
HSP70/HSPA5↑,
P53↑, thymoquinone can induce apoptosis in MCF-7 breast cancer cells via the up-regulation of p53 expression
miR-34a↑, Thymoquinone significantly increased the expression of miR-34a via p53, and down-regulated Rac1 expression
Rac1↓,
TumCCA↑, In hepatic carcinoma, thymoquinone induced cell cycle arrest and apoptosis by repressing the Notch signaling pathway
NOTCH↓,
NF-kB↓, Evidence revealed that thymoquinone suppresses tumor necrosis factor (TNF-α)-induced NF-kappa B (NF-κB) activation
IκB↓, consequently inhibits the activation of I kappa B alpha (I-κBα) kinase, I-κBα phosphorylation, I-κBα degradation, p65 phosphorylation
p‑p65↓,
IAP1↓, down-regulated the expression of NF-κB -regulated antiapoptotic gene products, like IAP1, IAP2, XIAP Bcl-2, Bcl-xL;
IAP2↑,
XIAP↓,
TNF-α↓, It also inhibited monocyte chemo-attractant protein-1 (MCP-1), TNF-α, interleukin (IL)-1β and COX-2, ultimately reducing the NF-κB activation in pancreatic ductal adenocarcinoma cells
COX2↓,
Inflam↓, indicating its role as an inhibitor of proinflammatory pathways
α-tubulin↓, Without affecting the tubulin levels in normal human fibroblast, thymoquinone induces degradation of α and β tubulin proteins in human astrocytoma U87 cells and in T lymphoblastic leukaemia Jurkat cells, and thus exerts anticancer activity
Twist↓, thymoquinone treatment inhibits TWIST1 promoter activity and decreases its expression in breast cancer cell lines; leading to the inhibition of epithelial-mesenchymal transition (EMT)
EMT↓,
mTOR↓, thymoquinone also attenuated mTOR activity, and inhibited PI3K/Akt signaling in bladder cancer
PI3K↓,
Akt↓,
BioAv↓, Thymoquinone is chemically hydrophobic, which causes its poor solubility, and thus bioavailability. bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min
ChemoSen↑, Some studies revealed that thymoquinone in combination with other chemotherapeutic drugs can show better anticancer activities
BioAv↑, Thymoquinone-loaded liposomes (TQ-LP) and thymoquinone loaded in liposomes modified with Triton X-100 (XLP) with diameters of about 100 nm were found to maintain stability, improve bioavailability and maintain thymoquinone’s anticancer activity
PTEN↑, Thymoquinone also induces apoptosis by up-regulating PTEN
chemoPv↑, A recent study showed that thymoquinone can potentiate the chemopreventive effect of vitamin D during the initiation phase of colon cancer in rat model
RadioS↑, thymoquinone also mediates radiosensitization and cancer chemo-radiotherapy
*Half-Life↝, Thymoquinone-loaded nanostructured lipid carrier (TQ-NLC) has been developed to improve its bioavailability (elimination half-life ~5 hours)
*BioAv↝, calculated absolute bioavailability of thymoquinone was reported ~58% with a lag time of ~23 min by Alkharfy et al.


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   ROS↓, 3,   ROS↑, 5,   ROS⇅, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   p‑AMPK↑, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 2,   Apoptosis↑, 2,   BAD↓, 1,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 3,   Casp7↑, 1,   Casp9↓, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   IAP1↓, 2,   IAP2↓, 1,   IAP2↑, 1,   iNOS↓, 1,   p‑JNK↓, 1,   Mcl-1↓, 2,   MDM2↓, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   p16↑, 1,   P53↑, 2,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   ERK↓, 1,   p‑ERK↓, 1,   FGF↓, 1,   HDAC10↑, 1,   miR-34a↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   p‑PI3K↓, 1,   PTEN↑, 1,   SCF↓, 1,   Wnt?, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   EFEMP↓, 1,   GLI2↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   MUC4↓, 1,   N-cadherin↓, 1,   Rac1↓, 1,   SPARC↓, 1,   TGF-β↓, 1,   Twist↓, 1,   Vim↓, 1,   α-tubulin↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   CXCc↓, 1,   IKKα↓, 1,   Inflam↓, 1,   IκB↓, 4,   IκB↑, 1,   p‑IκB↓, 3,   NF-kB↓, 7,   p50↓, 2,   p65↓, 2,   p‑p65↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   Dose↝, 1,   eff↑, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 2,   EGFR↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   ChemoSideEff↓, 1,   neuroP↑, 1,   TumVol↓, 1,  
Total Targets: 105

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 2,  

Cell Death ⓘ

iNOS↓, 1,   p‑JNK↓, 1,   MAPK↓, 1,   p‑p38↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Migration ⓘ

ARG↑, 1,   TGF-β1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

p‑IKKα↓, 1,   IL1↓, 1,   IL10↑, 1,   IL4↑, 1,   IL6↓, 1,   p‑IκB↓, 1,   MyD88↓, 1,   NF-kB↓, 1,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   cognitive↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 28

Scientific Paper Hit Count for: IκB, IκB kinase(α)
2 Rosmarinic acid
1 Baicalein
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Quercetin
1 Docetaxel
1 Magnolol
1 Magnetic Field Rotating
1 Magnetic Fields
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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