IKKα Cancer Research Results

IKKα, IκB kinase alpha): Click to Expand ⟱

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Expression of genes involved in nuclear factor (NF)-kappaB activation (NF-κB, IKKα) IKKα (IκB kinase alpha) is a critical component of the NF-κB signaling pathway, which plays a significant role in regulating immune responses, inflammation, and cell survival.
The NF-κB pathway, activated by IKKα, can lead to the production of pro-Inhibitors of the NF-κB pathway, including those targeting IKKα, are being investigated for their potential to treat various cancers.inflammatory cytokines that may create a tumor-promoting microenvironment.

Scientific Papers found: Click to Expand⟱

3167-

Ash,

Withaferin A Inhibits the Proteasome Activity in Mesothelioma In Vitro and In Vivo

in-vitro,

MM,

H226

0-5uM

TumCP↓, WA inhibits MPM cell proliferation
cMyc↓, Among the genes that were down-regulated included cell growth and metastasis-promoting oncogenes c-myc, c-fos, c-jun, while tissue inhibitor of metallopeptidases (TIMP)-2 was significantly upregulated
cFos↓,
cJun↓,
TIMP2↑,
Vim↓, WA exposure caused reduced levels of vimentin at 24 h of treatment.
ROS↑, WA treatment generated reactive oxygen species (ROS), causing cell death in HL-60 cells
BAX↑, Consistent with these findings, we found that WA treatments increased pro-apoptotic protein Bax and NF-κB inhibitory protein IκB-α in the patient derived MPM cells.
IKKα↑,
Casp3↑, Indeed, WA treatment induced caspase-3 activation, PARP cleavage,
cl‑PARP↑,

2599-

Ba,

Baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting PI3K/AKT pathway in vivo and vitro

in-vitro,

BC,

MCF-7

0, 10, 20, and 40 µM

14uM

 IC50 values of baicalein at 24, 48, and 72 hours were 51.06, 22.16, and 13.98 µM

in-vitro,

BC,

MDA-MB-231

60.12, 27.98, and 19.01 µM

in-vivo,

NA,

Female BALB/c nude mice

TumCP↓, baicalein has the potential to suppress cell proliferation, induce apoptosis and autophagy of breast cancer cells in vitro and in vivo.
Apoptosis↑,
p‑Akt↓, baicalein significantly downregulated the expression of p-AKT, p-mTOR, NF-κB, and p-IκB
p‑mTOR↓,
NF-kB↓,
p‑IKKα↓,
IKKα↑, while enhancing the expression of IκB in MCF-7 and MDA-MB-231
PI3K↓, baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting the PI3K/AKT signaling pathway in vivo and vitro
MMP↓, increasing dose of baicalein, the ΔΨm was decreased in MCF-7 and MDA-MB-231 cells.
TumAuto↑, Baicalein induces autophagy in MCF-7 and MDA-MB-231 cells
TumVol↓, demonstrated that the growth, volume, and weight of tumors were significantly suppressed in the baicalein-treated group compared with the control group
TumW↓,

2728-

BetA,

Betulinic acid as new activator of NF-kappaB: molecular mechanisms and implications for cancer therapy

in-vitro,

Var,

NF-kB↑, BetA activates NF-kappaB in a variety of tumor cell lines.
IKKα↑, BetA-induced NF-kappaB activation involved increased IKK activity
eff↓, NF-kappaB inhibitors in combination with BetA would have no therapeutic benefit or could even be contraproductive in certain tumors, which has important implications for the design of BetA-based combination protocols.

2496-

Fenb,

Impairment of the Ubiquitin-Proteasome Pathway by Methyl N-(6-Phenylsulfanyl-1H-benzimidazol-2-yl)carbamate Leads to a Potent Cytotoxic Effect in Tumor Cells

in-vitro,

NSCLC,

A549

1.6 μm

in-vitro,

NSCLC,

H460

1.2 uM

TumCG↓, We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells.
selectivity↑, but not normal cells
P53↑, A number of apoptosis regulatory proteins that are normally degraded by the ubiquitin-proteasome pathway like cyclins, p53, and IκBα were found to be accumulated in FZ-treated cells.
IKKα↑,
ER Stress↑, FZ induced distinct ER stress-associated genes like GRP78, GADD153, ATF3, IRE1α, and NOXA in these cells.
GRP78/BiP↑,
CHOP↑,
ATF3↑,
IRE1↑,
NOXA↑,
ROS↑, fenbendazole induced endoplasmic reticulum stress, reactive oxygen species production, decreased mitochondrial membrane potential, and cytochrome c release that eventually led to cancer cell death.
MMP↓,
Cyt‑c↑,
selectivity↑, treatment of human lung cancer cell lines with fenbendazole (FZ)3 induces apoptotic cell death, whereas primary normal cells in culture remain widely unaffected.
eff↝, The growth-inhibitory action of FZ in H460 and A549 cells was also compared with the Food and Drug Administration-approved proteasomal inhibitor bortezomib, and the results showed that the activities of both of the compounds were comparable

2844-

FIS,

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

in-vitro,

OS,

U2OS

tumCV↓, Fisetin at 20-100 µM effectively reduced the viability of OS cells, and induced apoptosis by signifi-cantly inducing the expression of Caspases- 3,-8 and -9 and pro-apoptotic proteins (Bax and Bad) with subsequent down-regulation of Bcl-xL and Bcl-2
Apoptosis↑,
Casp3↑,
Casp8↑,
Casp9↑,
BAX↑,
BAD↑,
Bcl-2↓,
Bcl-xL↓,
PI3K↓, inhibited PI3K/Akt pathway and ERK1/2,
Akt↓,
ERK↓,
p‑JNK↑, it caused enhanced expressions of p-JNK, p-c-Jun and p-p38
p‑cJun↑,
p‑p38↑,
ROS↑, Fisetin-induced ROS generation and decrease in mitochondrial membrane potential
MMP↓, noticeable decline of mitochondrial transmembrane potential (ΔΨm) in a dose-dependent manner
mTORC1↓, fisetin at various concentrations (20-100 μM) caused a significant (p<0.05) decrease in the level of p-Akt and mTORC1 (an important effector protein of Akt), while up-regulated PTEN.
PTEN↑,
p‑GSK‐3β↓, Level of phosphorylated glycogensynthase kinase 3ǃ (GSK3ǃ), (a serine/threonine kinase) and cyclin D1 were potentially decreased by fisetin which is in line with raised non-phosphorylated levels of GSK3ǃ
GSK‐3β↑,
NF-kB↓, Down-regualtion of NF-κB along with significant up-regulations in IκB upon fisetin treatment correlates with the down-regulation of p-Akt levels.
IKKα↑,
Cyt‑c↑, activates the efflux of cytochrome C

2884-

HNK,

Honokiol inhibits EMT-mediated motility and migration of human non-small cell lung cancer cells in vitro by targeting c-FLIP

in-vitro,

Lung,

A549

in-vitro,

Lung,

H460

EMT↓, HNK inhibits EMT-mediated motility and migration of human NSCLC cells in vitro by targeting c-FLIP,
cFLIP↓,
N-cadherin↓, increased c-FLIP, N-cadherin (a mesenchymal marker), snail (a transcriptional modulator) and p-Smad2/3 expression, and decreased IκB levels in the cells; these changes were abrogated by co-treatment with HNK (30 μmol/L)
Snail↓,
p‑SMAD2↓,
p‑SMAD3↓,
IKKα↑,
TumCMig↓, HNK inhibits the migration of A549 and H460 cells induced by TNF-α+TGF-β1

2868-

HNK,

Honokiol: A review of its pharmacological potential and therapeutic insights

Review,

Var,

Review,

Sepsis,

*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2Î±, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786â0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice

2385-

MET,

Metformin activates chaperone-mediated autophagy and improves disease pathologies in an Alzheimer disease mouse model

in-vitro,

AD,

in-vitro,

NA,

HEK293

in-vivo,

NA,

APP/PS1 mice develop AD-like cognitive deficits

in-vitro,

NA,

SH-SY5Y

*HK2↓, Metformin also induced degradation of two endogenous CMA substrates—HK2 and PKM2 (pyruvate kinase isozyme type M2), at both 20 mmol/L and 20 µmol/L doses of the drug
*PKM2↓,
*Dose↝, We chose these two doses due to the robustness of the 20 mmol/L dose and due to the clinical relevance of the 20 µmol/L dose, as the Metformin serum concentrations in patients receiving this drug are ~20 µmol/L
IKKα↑, Metformin activates TAK1-IKKα/β signaling
memory↑, Metformin-treated APP/PS1 mice showed improved learning and spatial memory
p‑Hsc70↑, Metformin treatment also significantly reduced the protein levels of APP and induced Hsc70 phosphorylation at Ser85, consistent with our findings in cell culture
APP↓, Metformin induced degradation of endogenous APP proteins in SH-SY5Y cell

1940-

PL,

Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways

in-vitro,

GBM,

LN229

1, 2, or 5 μM, 10uM

in-vitro,

GBM,

U87MG

ROS↑, demonstrated that PL induced ROS accumulation in scratched LN229 cells.
GSH↓, reduced glutathione
p38↑, activated p38 and JNK, increased IκBα
JNK↑,
IKKα↑,
NF-kB↓, suppressed NFκB in LN229 cells after scratching
eff↓, All the biological effects of PL in scratched LN229 cells were completely abolished by the antioxidant N-acetyl-L-cysteine (NAC).

1195-

SM,

Salvia miltiorrhiza polysaccharide activates T Lymphocytes of cancer patients through activation of TLRs mediated -MAPK and -NF-κB signaling pathways

in-vitro,

Lung,

A549

in-vitro,

Liver,

HepG2

in-vitro,

CRC,

HCT116

T-Cell↑,
TumCP∅, SMP showed no effect on the proliferation of the tumor cells
IL4↑,
IL6↑,
IFN-γ↑,
TLR4↑,
TLR1↑,
TLR2↑,
p‑JNK↑,
p‑ERK↑,
IKKα↑,

Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GSH↑, 1, HO-1↑, 1, NRF2↑, 1, ROS↓, 2,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, HK2↓, 1, NADPH↓, 1, PKM2↓, 1,

Cell Death ⓘ

Casp3↓, 1,

Migration ⓘ

p‑Rac1↓, 1,

Barriers & Transport ⓘ

P-gp↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IKKα↑, 1, IL10↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,

Drug Metabolism & Resistance ⓘ

Dose↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 1, IL6↓, 1,

Functional Outcomes ⓘ

cardioP↑, 1, hepatoP↑, 1, neuroP↑, 1, RenoP↑, 1,
Total Targets: 30

Scientific Paper Hit Count for: IKKα, IκB kinase alpha)

2 Honokiol
1 Ashwagandha(Withaferin A)
1 Baicalein
1 Betulinic acid
1 Fenbendazole
1 Fisetin
1 Metformin
1 Piperlongumine
1 Salvia miltiorrhiza

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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:156  State#:%  Dir#:2
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IKKα Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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