PYCR1 Cancer Research Results

PYCR1, Pyrroline-5-Carboxylate Reductase 1: Click to Expand ⟱
Source:
Type:
Pyrroline-5-Carboxylate Reductase 1 (PYCR1) is an enzyme that catalyzes the final step in proline biosynthesis by reducing pyrroline-5-carboxylate to proline. This enzyme plays an integral role in cellular metabolism and redox balance. In the context of cancer, PYCR1 has emerged as a notable factor, with its expression levels often correlating with tumor progression and patient prognosis.

-Numerous studies have found that PYCR1 is overexpressed in a variety of tumor types, including breast cancer, lung cancer, liver cancer, and others.
Elevated PYCR1 expression is thought to provide tumor cells with a survival advantage by contributing to anabolic metabolism and helping to mitigate oxidative stress.
Scientific Papers found: Click to Expand⟱
1654- FA,    Molecular mechanism of ferulic acid and its derivatives in tumor progression
- Review, Var, NA
AntiCan↑, FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity,
Inflam↓,
RadioS↑,
ROS↑, FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS)
Apoptosis↑,
TumCCA↑, G0/G1 phase
TumCMig↑, inducing autophagy; inhibiting cell migration, invasion, and angiogenesis
TumCI↓,
angioG↓,
ChemoSen↑, synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions.
ChemoSideEff↓,
P53↑, FA could increase the expression level of p53 in MIA PaCa-2 pancreatic cancer cells
cycD1/CCND1↓, while reducing the expression levels of cyclin D1 and cyclin-dependent kinase (CDK) 4/6.
CDK4↓,
CDK6↓,
TumW↓, FA treatment was found to reduce tumor weight in a dose-dependent manner, increase miR-34a expression, downregulate Bcl-2 protein expression, and upregulate caspase-3 protein expression
miR-34a↑,
Bcl-2↓,
Casp3↑,
BAX↑,
β-catenin/ZEB1↓, isoferulic acid dose-dependently downregulated the expression of β-catenin and MYC proto-oncogene (c-Myc), inducing apoptosis
cMyc↓,
Bax:Bcl2↑, FXS-3 can inhibit the activity of A549 cells by upregulating the Bax/Bcl-2 ratio
SOD↓, After treatment with FA, Cao et al. [40] observed an increase in ROS production and a decrease in superoxide dismutase activity and glutathione content in EC-1 and TE-4 oesophageal cancer cells
GSH↓,
LDH↓, FA could promote the release of lactate dehydrogenase (LDH)
ERK↑, A can activate the ERK1/2 pathway
eff↑, conjugated zinc oxide nanoparticles with FA (ZnONPs-FA) to act on hepatoma Huh-7 and HepG2 cells. The results showed that ZnONPs-FA could induce oxidative DNA damage and apoptosis by inducing ROS production.
JAK2↓, by inhibiting the JAK2/STAT6 immune signaling pathway
STAT6↓,
NF-kB↓, thus inhibiting the activation of NF-κB
PYCR1↓, FA can target PYCR1 and inhibit its enzyme activity in a concentration-dependent manner.
PI3K↓, FA inhibits the activation of the PI3K/AKT pathway
Akt↓,
mTOR↓, FA could significantly reduce the expression level of mTOR mRNA and Ki-67 protein in A549 lung cancer graft tissue
Ki-67↓,
VEGF↓,
FGFR1↓, FA is a novel FGFR1 inhibitor
EMT↓, FA can inhibit EMT
CAIX↓, selectively inhibit CAIX
LC3II↑, Autophagy vacuoles and increased LC3-II and p62 autophagy proteins were observed after treatment with this compound
p62↑,
PKM2↓, FA could inhibit the expression of PKM2 and block aerobic glycolysis
Glycolysis↓,
*BioAv↓, FA has poor solubility in water and a poor ability to pass through biological barriers [118]; therefore, the extent to which it is metabolized in vivo after oral administration is largely unknown

2224- SK,    Shikonin induces apoptosis and autophagy via downregulation of pyrroline-5-carboxylate reductase1 in hepatocellular carcinoma cells
- in-vitro, HCC, SMMC-7721 cell - in-vitro, HCC, HUH7 - in-vitro, HCC, HepG2
PYCR1↓, SK may induce apoptosis and autophagy by reducing the expression of PYCR1 and suppressing PI3K/Akt/mTOR
PI3K↓,
Akt↓,
mTOR↓,
eff↑, SK reinforces its anti-tumor effects by downregulating PYCR1 in HCC cells


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 ⓘ

GSH↓, 1,   PYCR1↓, 2,   ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

FGFR1↓, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↓, 1,   cMyc↓, 1,   Glycolysis↓, 1,   LDH↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↑, 1,   miR-34a↑, 1,   mTOR↓, 2,   PI3K↓, 2,   STAT6↓, 1,  

Migration ⓘ

Ki-67↓, 1,   TumCI↓, 1,   TumCMig↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   ChemoSideEff↓, 1,   TumW↓, 1,  
Total Targets: 46

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: PYCR1, Pyrroline-5-Carboxylate Reductase 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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1158  State#:%  Dir#:1
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