TumAuto Cancer Research Results

TumAuto, Tumor autophagy: Click to Expand ⟱
Source: HalifaxProj(activate)
Type:
Autophagy genes, including Atg3, Atg5, Atg6, Atg7, Atg10, Atg12, and Atg17.
Tumor autophagy refers to the process by which cancer cells degrade and recycle cellular components through autophagy, a cellular mechanism that helps maintain homeostasis and respond to stress. Autophagy can have dual roles in cancer, acting as both a tumor suppressor and a promoter, depending on the context.
Authophagy is the process used by cancer cells to “self-eat” to survive. Authophagy can be both good and bad. If authophagy is prolonged this will become a lethal process to cancer. On the other hand, for a short while (e.g. during chemotheraphy, radiotheraphy, etc.) authophagy is used by cancer cells to survive.
For example, Chloroquine is a blocker of autophagy and has been used in a lab setting to dramatically enhance tumor response to radiotherapy, chemotherapy.
Scientific Papers found: Click to Expand⟱
6881- FA,    Potential Therapeutic Efficacy of Ferulic Acid and Its Derivatives in the Management of Cancers: A Comprehensive Analysis With Mechanistic Insight
- Review, Var, NA
ROS↑, FA showed promising anticancer activity through underlying mechanisms, including induction of oxidative stress, cytotoxic effect, cell cycle arrest, apoptotic effect, suppression of invasion and migration, antiproliferative effect, autophagy, and gen
TumCCA↑,
TumCI↓,
TumCMig↓,
TumCP↓,
BioAv↑, FA, indicating lower oral bioavailability is affected by the liver's fast conjugation process; this limitation is overcome by applying a nanoformulation of FA.
BioAv↑, medication's bioavailability is 100% when administered intravenously (IV)
TP53↑, FA could impede cell growth by upregulating the gene expression of TP53 and downregulating the gene expression of CDK2, CDK4, and CDK6 in prostate cancer PC-3 cells, resulting in cell cycle arrest in PC-3 cells
CDK2↓,
CDK4↓,
CDK6↓,
JAK2↓, blocking the JAK2/STAT6 immune signaling pathway
STAT6↓,
tyrosinase↓, FA could also decrease tyrosinase activity by directly binding to enzymes
p‑Akt↓, FA lowered phosphorylation of AKT and PI3K in CaSki cells in a dose-dependent way,
p‑PI3K↓,
mTOR↓, FA reduced the amount of mTOR mRNA and Ki-67 protein in A549 lung
Ki-67↓,
Casp3↑, increased the levels of caspase-3 protein
proCasp8↑, FA elevated pro-caspase-3, pro-caspase-8, and pro-caspase-9 and PARP cleavage, Bax, and ROS and decreased Bcl-2, Mcl-1, AKT, and PI3K pathway levels in a dose-dependent way
cl‑PARP↑,
BAX↑,
Bcl-2↓,
Mcl-1↓,
MMP9↓, reducing cell invasion, MMP9 mRNA expression, and cyclin D1 and cyclin E levels
cycD1/CCND1↓,
cycE/CCNE↓,
PINK1↑, FA (100 μg/mL) enhanced apoptosis via increasing PINK-1, Parkin and reducing the MMP expression
PARK2↑,
MMP↓,
CycD3↓, reducing the gene expressions of CCND1, CCND2, CCND3, CDK2, CDK4, and CDK6 level in PC-3 cells
TumAuto⇅, FA has shown anticancer activity via the increase and decrease of autophagy in different types of cancer.
eff↑, by combining with other compounds like 2-deoxy-D-glucose (2DG) [164], epirubicin, gamma radiation [165], aspirin, thyoquinine [166], phenolic and flavonoids, P-coumaric acid [167], 4-vinylguaiacol, caffeic [168], coumaric, and gemcitabine [169].
eff↑, FA and aspirin could trigger apoptotic cell death, p-RB, p21, and p-ERK1/2, cytotoxicity and reduce PCNA and MKI67, growth of tumor in pancreatic cancer.
ALAT↓, figure 5
AST↓,
ALP↓,
VEGF↓,
MMPs↓,
angioG↓,

1962- GamB,  HCQ,    Gambogic acid induces autophagy and combines synergistically with chloroquine to suppress pancreatic cancer by increasing the accumulation of reactive oxygen species
- in-vitro, PC, NA
LC3II↑, Gambogic acid induced the expression of LC3-II and Beclin-1 proteins in pancreatic cancer cells, whereas the expression of P62 showed a decline.
Beclin-1↑,
p62↓,
MMP↓, gambogic acid reduced the mitochondrial membrane potential and promoted ROS production, which contributed to the activation of autophagy
ROS↑,
TumAuto⇅, up by GamB, down by HCQ
eff↑, inhibition of autophagy by chloroquine further reduced the mitochondrial membrane potential and increased the accumulation of ROS


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

PARK2↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   PINK1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   proCasp8↑, 1,   Mcl-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto⇅, 2,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   CycD3↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

mTOR↓, 1,   p‑PI3K↓, 1,   STAT6↓, 1,   tyrosinase↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

JAK2↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   Ki-67↓, 1,   TP53↑, 1,  
Total Targets: 44

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumAuto, Tumor autophagy
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#:321  State#:%  Dir#:3
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