ASK1 Cancer Research Results
ASK1, Apoptosis Signal-regulating Kinase 1: Click to Expand ⟱
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ASK1 (Apoptosis Signal-regulating Kinase 1) is a protein kinase that plays a crucial role in cell signaling pathways, particularly in the regulation of apoptosis (programmed cell death) and cell survival.
ASK1 if often overexpressed and has been linked to tumor progression and poor prognosis.
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Scientific Papers found: Click to Expand⟱
Ca+2↑, MDA-MB-231 ↑Ca2+
MMP2↓, MDA-MB-231 ↓MMP-2/9
MMP9↓,
Vim↓, ↓Vimentin, ↓SNAIL, ↑E-cadherin, ↓Wnt1, ↓β-catenin
Snail↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,
p‑Akt↓, MCF-7 ↓p-Akt, ↓p-mTOR, ↓NF-κB
p‑mTOR↓,
NF-kB↓,
i-ROS↑, MCF-7 ↑Intracellular ROS, ↓Bcl-2, ↑Bax, ↑cytochrome c, ↑caspase-3/9
Bcl-2↓,
BAX↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
STAT3↓, 4T1, MDA-MB-231 ↓STAT3, ↓ IL-6
IL6↓,
MMP2↓, HeLa ↓MMP-2, ↓MMP-9
MMP9↓,
NOTCH↓, ↓Notch 1
PPARγ↓, ↓PPARγ
p‑NRF2↓, HCT-116 ↓p-Nrf2
HK2↓, ↓HK2, ↓LDH-A, ↓PDK1, ↓glycolysis, PTEN/Akt/HIF-1α regulation
LDHA↓,
PDK1↓,
Glycolysis↓,
PTEN↑, Furthermore, baicalein inhibited hypoxia-induced Akt phosphorylation by promoting PTEN accumulation, thereby attenuating hypoxia-inducible factor-alpha ( HIF-1a) expression in AGS cells.
Akt↓,
Hif1a↓,
MMP↓, SGC-7901 ↓ΔΨm
VEGF↓, ↓VEGF, ↓VEGFR2
VEGFR2↓,
TOP2↓, ↓Topoisomerase II
uPA↓, ↓u-PA, ↓TIMP1, ↓TIMP2
TIMP1↓,
TIMP2↓,
cMyc↓, ↓β-catenin, ↓c-Myc, ↓cyclin D1, ↓Axin-2
TrxR↓, EL4 ↓Thioredoxin reductase, ↑ASK1,
ASK1↑,
Vim↓, ↓vimentin
ZO-1↑, ↑ZO-1
E-cadherin↑, ↑E-cadherin
SOX2↓, PANC-1, BxPC-3, SW1990 ↓Sox-2, ↓Oct-4, ↓SHH, ↓SMO, ↓Gli-2
OCT4↓,
Shh↓,
Smo↓,
Gli1↓,
N-cadherin↓, ↓N-cadherin
XIAP↓, ↓XIAP
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in-vitro, |
BC, |
SUM159 |
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in-vitro, |
BC, |
4T1 |
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PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells
HDAC↓, Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).
TumCCA↑, phenylbutyrate treatment that results in reduced proliferation and cell-cycle arrest in G1 or G2 phases.
P21↑, common sequela of phenylbutyrate treatment is the upregulation of p21,
Dose↝, In prostate cancer, phenylbutyrate at clinically achievable concentrations (0.1 mM-8 mM),
Telomerase↓, butyrate or its derivatives was also evident in several other types of cancers and was associated with loss of telomerase activity
IGFBP3↑, Upregulation of insulin-like growth factor binding protein 3 (IGFBP-3) is another unique antiproliferative mechanism of sodium butyrate in breast cancer cells
p‑p38↑, Phenylbutyrate and its derivatives upregulated p21, gelsolin, phosphorylated p38, JNK, and ERK (MAPK pathway members), Bax, caspases-3,
JNK↑,
ERK↑,
BAX↑,
Casp3↑,
Bcl-2↓, downregulated Bcl-X L , Bcl-2, cytochrome c, FAK, and survivin
Cyt‑c↝,
FAK↓,
survivin↓,
VEGF↓, Butyrate treatment reduced the level of vascular endothelial growth factor (VEGF)
angioG↓,
DNArepair↓, Inhibition of DNA Repair.
TumMeta↓,
HSP27↑, Moreover, butyrate treatment in colorectal cancer cells resulted in an acute stress response that was associated with HSP27 activation, activation of ASK1 (MAP3K) and p38 MAPK pathway consequently.
ASK1↑,
ROS↑, Also it resulted in elevated cellular levels of reactive oxygen species (ROS) in oral and tongue cancer cells.
eff↑, phenylbutyrate enhanced the cytotoxicity of temozolamide in malignant glioma cells via suppression of the endoplasmic reticulum stress revealed by the decreased expression of GRP78 and GADD153.
ER Stress↓,
GRP78/BiP↓,
CHOP↑, GADD153
AR↓, Sodium butyrate treatment of prostate cancer cells was associated with downregulation of androgen receptor
other?, lots of references in this paper.
GSH↓, high Qu concentration, causes a reduction in GSH content
ROS↑, in tumor cells
TumCCA↑, Depending on the cell type and tumor origin, Qu is able to block the cell cycle at G2/M or at the G1/S transition
Ca+2↑, Qu treatment increases cytosolic Ca2+ levels
MMP↓,
Casp3↑,
Casp8↑,
Casp9↑,
β-catenin/ZEB1↓,
AMPKα↑,
ASK1↑,
p38↑,
TRAIL↑, Qu is a potent enhancer of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, through the induction of the expression of death receptor (DR)-5, a phenomenon that specifically occurs in prostate cancer cells
DR5↑,
cFLIP↓,
Apoptosis↑, tumor cell lines are prone to cell-cycle arrest and apoptosis at Qu concentrations that have no or little effect on non-transformed cells ****
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, hyperG↓, 1, p‑NRF2↓, 1, ROS↑, 3, i-ROS↑, 1, TrxR↓, 1,
Metal & Cofactor Biology ⓘ
KLF5↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 2, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, PDK1↓, 1, PPARγ↓, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 2, p‑Akt↓, 1, Apoptosis↑, 1, ASK1↑, 4, BAX↑, 2, Bcl-2↓, 2, BIM↑, 1, Casp3↑, 4, Casp8↑, 1, Casp9↑, 2, cFLIP↓, 1, Cyt‑c↑, 1, Cyt‑c↝, 1, DR5↑, 1, JNK↑, 1, p38↑, 1, p‑p38↑, 1, survivin↓, 1, Telomerase↓, 1, TRAIL↑, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1,
Transcription & Epigenetics ⓘ
other?, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↓, 1, GRP78/BiP↓, 1, HSP27↑, 1,
DNA Damage & Repair ⓘ
DNArepair↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK4↑, 2, P21↑, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, Gli1↓, 1, p‑GSK‐3β↑, 1, HDAC↓, 1, IGFBP3↑, 1, mTOR↑, 2, p‑mTOR↓, 1, Nanog↓, 1, NOTCH↓, 1, OCT4↓, 2, PI3K↑, 2, PTEN↑, 1, Shh↓, 1, Smo↓, 1, SOX2↓, 1, STAT3↓, 1, TOP2↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
Ca+2↑, 2, E-cadherin↑, 2, FAK↓, 1, KLF2↓, 1, MMP2↓, 2, MMP9↓, 2, N-cadherin↓, 1, PKA↓, 1, Snail↓, 1, TIMP1↓, 1, TIMP2↓, 1, TumMeta↓, 1, uPA↓, 1, Vim↓, 2, ZO-1↑, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 1, VEGF↓, 2, VEGFR2↓, 1,
Immune & Inflammatory Signaling ⓘ
IL6↓, 1, NF-kB↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1, CDK6↑, 2,
Drug Metabolism & Resistance ⓘ
Dose↝, 1, eff↑, 4, eff∅, 1,
Clinical Biomarkers ⓘ
AR↓, 1, BG↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
TumVol↓, 1,
Total Targets: 97
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: ASK1, Apoptosis Signal-regulating Kinase 1
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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