Cyt‑c Cancer Research Results

Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.


Ovarian, Ovarian Cancer: Click to Expand ⟱
Ovarian Cancer


Scientific Papers found: Click to Expand⟱
5977- AgNPs,  CDT,    Silver Nitroprusside as an Efficient Chemodynamic Therapeutic Agent and a Peroxynitrite nanogenerator for Targeted Cancer Therapy
- in-vivo, Ovarian, A2780S - NA, Ovarian, SKOV3
Fenton↑, ROS↑, eff↑, angioG↓, p‑Akt↓, EPR↑, selectivity↑, selectivity↑, eff↑, Cyt‑c↑, HO-1↑,
397- AgNPs,  GEM,    Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment
- in-vitro, Ovarian, A2780S
P53↑, P21↑, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, Bcl-2↓, ROS↑, MMP↓,
1585- Citrate,    Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S - in-vitro, Nor, HEK293
Apoptosis↑, Ferroptosis↑, Ca+2↓, CaMKII ↓, Akt↓, mTOR↓, Hif1a↓, ROS↑, ChemoSen↑, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, Cyt‑c↑, GlucoseCon↓, lactateProd↓, Pyruv↓, GLUT1↓, HK2↓, PFKP↓, Glycolysis↓, Hif1a↓, p‑Akt↓, p‑mTOR↓, Iron↑, lipid-P↑, MDA↑, ROS↑, H2O2↑, mtDam↑, GSH↓, GPx↓, GPx4↓, NADPH/NADP+↓, eff↓, FTH1↓, LC3‑Ⅱ/LC3‑Ⅰ↑, NCOA4↑, eff↓, TumCG↓,
1959- GamB,    Gambogic acid induces GSDME dependent pyroptotic signaling pathway via ROS/P53/Mitochondria/Caspase-3 in ovarian cancer cells
- in-vitro, Ovarian, NA - in-vivo, NA, NA
AntiCan↑, Pyro↑, tumCV?, CellMemb↓, cl‑Casp3↑, GSDME-N↑, ROS?, p‑P53↑, eff↓, MMP↓, Bcl-2↓, BAX↑, mtDam↑, Cyt‑c↑, TumCG↓, CD4+↑, CD8+↑,
5327- TFdiG,    Theaflavin-3, 3'-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells
- in-vitro, Ovarian, A2780S
TumCG↓, selectivity↑, TumCCA↑, Apoptosis↑, P53↑, BAX↑, BAD↑, cl‑Casp3↑, p‑Akt↓, MDM2↓, MMP↓, Cyt‑c↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Fenton↑, 1,   Ferroptosis↑, 1,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 1,   H2O2↑, 1,   HO-1↑, 1,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADPH/NADP+↓, 1,   ROS?, 1,   ROS↑, 4,  

Metal & Cofactor Biology

FTH1↓, 1,   NCOA4↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 3,   mtDam↑, 2,  

Core Metabolism/Glycolysis

GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PFKP↓, 1,   Pyruv↓, 1,  

Cell Death

Akt↓, 1,   p‑Akt↓, 3,   Apoptosis↑, 2,   BAD↑, 1,   Bak↑, 1,   BAX↑, 4,   Bcl-2↓, 3,   Casp3↑, 2,   cl‑Casp3↑, 2,   Casp9↑, 2,   Cyt‑c↑, 5,   Ferroptosis↑, 1,   GSDME-N↑, 1,   MDM2↓, 1,   Pyro↑, 1,  

Kinase & Signal Transduction

CaMKII ↓, 1,  

Transcription & Epigenetics

tumCV?, 1,  

Autophagy & Lysosomes

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

DNA Damage & Repair

P53↑, 2,   p‑P53↑, 1,  

Cell Cycle & Senescence

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

mTOR↓, 1,   p‑mTOR↓, 1,   TumCG↓, 3,  

Migration

Ca+2↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   EPR↑, 1,   Hif1a↓, 2,  

Barriers & Transport

CellMemb↓, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling

CD4+↑, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   eff↓, 3,   eff↑, 2,   selectivity↑, 3,  

Functional Outcomes

AntiCan↑, 1,  

Infection & Microbiome

CD8+↑, 1,  
Total Targets: 61

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
2 Silver-NanoParticles
1 chemodynamic therapy
1 Gemcitabine (Gemzar)
1 Citric Acid
1 Gambogic Acid
1 Aflavin-3,3′-digallate
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:20  Cells:%  prod#:%  Target#:77  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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