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.
Bladder, Bladder Cancer: Click to Expand ⟱
Bladder Cancer
Scientific Papers found: Click to Expand⟱
5130- ART/DHA,    Dihydroartemisinin Induces Apoptosis in Human Bladder Cancer Cell Lines Through Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cytochrome C Pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, eff↓, Apoptosis↑, Casp3↑, ROS↑, Cyt‑c↑, MMP↓, Bcl-2↓, BAX↑, MOMP↑, TumCG↓,
1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, eff↓, TumW↓, TumW↓, angioG↓, *toxicity↓, GutMicro↝, AntiCan↑, ROS↑, MMP↓, Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, Casp8∅, cl‑PARP↑, TRAIL↑, DR5↑, eff↓, NRF2↑, ER Stress↑, COX2↓, EGFR↓, HER2/EBBR2↓, ChemoSen↑, NF-kB↓, TumCCA?, p‑Akt↓, p‑mTOR↓, p70S6↓, p19↑, P21↑, CD44↓, CSCs↓,
1482- SFN,    Sulforaphane induces apoptosis in T24 human urinary bladder cancer cells through a reactive oxygen species-mediated mitochondrial pathway: the involvement of endoplasmic reticulum stress and the Nrf2 signaling pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, Apoptosis↑, Cyt‑c↑, Bax:Bcl2↑, Casp9↑, Casp3↑, Casp8∅, cl‑PARP↑, ROS↑, MMP↓, eff↓, ER Stress↑, p‑NRF2↑, HO-1↑,
3416- TQ,    Thymoquinone induces apoptosis in bladder cancer cell via endoplasmic reticulum stress-dependent mitochondrial pathway
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, 253J - in-vitro, Nor, SV-HUC-1
TumCP↓, Apoptosis↑, ER Stress↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp7↑, cl‑PARP↑, Cyt‑c↑, PERK↑, IRE1↑, ATF6↑, p‑eIF2α↑, ATF4↑, GRP78/BiP↑, CHOP↑,
2279- VitK2,    Vitamin K2 Induces Mitochondria-Related Apoptosis in Human Bladder Cancer Cells via ROS and JNK/p38 MAPK Signal Pathways
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, J82 - in-vitro, Nor, HEK293 - in-vitro, Nor, L02 - in-vivo, NA, NA
MMP↓, Cyt‑c↑, Casp3↑, p‑JNK↑, p‑p38↑, ROS↑, eff↓, tumCV↓, selectivity↑, *toxicity↓, TumVol↓,

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 ⓘ

HO-1↑, 1,   NRF2↑, 1,   p‑NRF2↑, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 4,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bax:Bcl2↑, 2,   Bcl-2↓, 1,   Casp3↑, 4,   cl‑Casp3↑, 1,   cl‑Casp7↑, 1,   Casp8∅, 2,   cl‑Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 5,   DR5↑, 1,   p‑JNK↑, 1,   MOMP↑, 1,   p‑p38↑, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   CHOP↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   IRE1↑, 1,   PERK↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 3,  

Cell Cycle & Senescence ⓘ

p19↑, 1,   P21↑, 1,   TumCCA?, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   HDAC↓, 1,   p‑mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,   EGFR↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↓, 5,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   GutMicro↝, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   TumVol↓, 1,   TumW↓, 2,  
Total Targets: 56

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 1

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
2 Sulforaphane (mainly Broccoli)
1 Artemisinin
1 Thymoquinone
1 Vitamin K2
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:32  Cells:%  prod#:%  Target#:77  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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