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.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
5272- 3BP,    The efficacy of the anticancer 3-bromopyruvate is potentiated by antimycin and menadione by unbalancing mitochondrial ROS production and disposal in U118 glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
Glycolysis↓, ROS↑, GPx↓, eff↓, OXPHOS↓, HK2↓, ATP↓, ROS↑, ER Stress↑, BioAv↓, Cyt‑c↑, eff↑,
5133- ART/DHA,    Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
AntiTum↑, tumCV↓, Apoptosis↓, MMP↓, Cyt‑c↑, Casp9↑, CHOP↑, GRP78/BiP↑, eIF2α↑, Casp12↑, ER Stress↑, TumAuto↑, ROS↑,
5584- BetA,    Betulinic acid induces apoptosis through a direct effect on mitochondria in neuroectodermal tumors
- in-vitro, GBM, A172 - in-vitro, GBM, U118MG - in-vitro, GBM, U251
Apoptosis↑, P53↑, Cyt‑c↑, AIF↑, Casp↑, AntiTum↑, MMP↓,
5835- CAP,    Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+-mediated mitochondrial pathway
- in-vitro, GBM, U251
tumCV↓, Apoptosis↑, selectivity↑, ROS↑, Ca+2↑, MMP↓, Cyt‑c↑, Casp↑, eff↑, MPT↑, ETC↓, Casp3↑, Casp9↑,
1976- EGCG,    Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cells
- in-vitro, GBM, U87MG
ROS↑, MMP↓, Casp3↑, Cyt‑c↑, Trx1↓, Ceru↓, IL6↓, IL8↓, MCP1↓, RANTES?, uPA↝, ROS↑,
1967- GamB,    Gambogic acid induces apoptotic cell death in T98G glioma cells
- in-vitro, GBM, T98G
BAX↑, AIF↑, Cyt‑c↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↓, Bcl-2↓, ROS↑,
2903- LT,    Luteolin induces apoptosis by ROS/ER stress and mitochondrial dysfunction in gliomablastoma
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vivo, NA, NA
ER Stress↑, ROS↑, PERK↑, eIF2α↑, ATF4↑, CHOP↑, Casp12↑, eff↓, UPR↑, MMP↓, Cyt‑c↑, Bcl-2↓, BAX↑, TumCG↓, Weight∅, ALAT∅, AST∅,
3493- MFrot,  MF,    Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubes
- in-vivo, GBM, NA
TumCD↑, MMP↓, Cyt‑c↑, Apoptosis↑, OS↑, DNAdam↑,
2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Bcl-2↓, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, ROS↑, lactateProd↑, Apoptosis↑, MPT↑, *selectivity↑, eff↑, MMP↓, selectivity↑, TCA?, H2O2↑, eff↑, *antiOx↑, H2O2↑, eff↓, GSH/GSSG↓, *toxicity∅, OS↑,
184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, mitResp↓, mtDam↑, Dose↝, MMP?, OCR↓, mt-H2O2↑, eff↓, SDH↓, Thiols↓, GSH↓, TumCD↑, Casp3↑, Casp7↑, MPT↑, Cyt‑c↑, selectivity↑, GSH/GSSG↓, ETC↓,
1735- SFN,    Activation of multiple molecular mechanisms for apoptosis in human malignant glioblastoma T98G and U87MG cells treated with sulforaphane
- in-vitro, GBM, T98G - in-vitro, GBM, U87MG
Apoptosis↑, Ca+2↑, Bax:Bcl2↑, cal2↑, Casp12↑, Casp9↑, Cyt‑c↑,
1346- SK,    An Oxidative Stress Mechanism of Shikonin in Human Glioma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, Hs683
NRF2↓, ROS↑, Apoptosis↑, Cyt‑c↑, GSH↓, MMP↓, P53↑, HO-1⇅,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ceru↓, 1,   GPx↓, 1,   GSH↓, 2,   GSH/GSSG↓, 2,   H2O2↑, 2,   mt-H2O2↑, 1,   HO-1⇅, 1,   NRF2↓, 1,   OXPHOS↓, 1,   ROS↑, 11,   Thiols↓, 1,   Trx1↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 1,   ETC↓, 2,   mitResp↓, 1,   MMP?, 1,   MMP↓, 9,   MPT↑, 3,   mtDam↑, 1,   OCR↓, 1,   SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT∅, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↑, 1,   TCA?, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Apoptosis↑, 6,   Bak↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Casp↑, 2,   Casp12↑, 3,   Casp3↑, 4,   cl‑Casp3↑, 1,   Casp7↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 4,   cl‑Casp9↑, 1,   Cyt‑c↑, 12,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   eIF2α↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 2,   cl‑PARP↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 2,   cal2↑, 1,   uPA↝, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   IL8↓, 1,   MCP1↓, 1,   RANTES?, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Dose↝, 1,   eff↓, 4,   eff↑, 4,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

ALAT∅, 1,   AST∅, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 2,   OS↑, 2,   Weight∅, 1,  
Total Targets: 74

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 3

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
3 Magnetic Field Rotating
3 Magnetic Fields
1 3-bromopyruvate
1 Artemisinin
1 Betulinic acid
1 Capsaicin
1 EGCG (Epigallocatechin Gallate)
1 Gambogic Acid
1 Luteolin
1 Sulforaphane (mainly Broccoli)
1 Shikonin
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:27  Cells:%  prod#:%  Target#:77  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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