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.
Scientific Papers found: Click to Expand⟱
5728- BF,    Effects of bufalin on the proliferation of human lung cancer cells and its molecular mechanisms of action
- in-vitro, Lung, A549
TumCP↓, we have demonstrated that bufalin suppressed the proliferation of human NSCLC A549 cell line in time- and dose-dependent manners.
Apoptosis↑, Bufalin induced the apoptosis and cell cycle arrest by affecting the protein expressions of Bcl-2/Bax, cytochrome c, caspase-3, PARP, p53, p21WAF1, cyclinD1, and COX-2 in A549 cells.
TumCCA↑,
Bcl-2↝,
BAX↝,
Cyt‑c↝,
Casp3↝,
PARP↝,
P21↝,
cycD1/CCND1↝,
COX2↝,
p‑VEGFR2↓, bufalin reduced the protein levels of receptor expressions and/or phosphorylation of VEGFR1, VEGFR2, EGFR and/or c-Met in A549 cells.
EGFR↓,
Akt↓, bufalin inhibited the protein expressions and phosphorylation of Akt, NF-κB, p44/42 MAPK (ERK1/2) and p38 MAPK in A549 cells.
NF-kB↓,
p44↓,

15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
- Review, Pca, NA
NF-kB↝, involve NF-κB, Akt, androgen receptors, and apoptosis pathways.
Akt↝, see figure 5
AR↝,
Apoptosis↝,
Bcl-2↝,
Casp3↝,
BAX↝,
P21↝,
ROS↝,
Bcl-xL↝,
JNK↝,
MMP2↝,
P53↝,
PSA↝,
VEGF↝,
COX2↝,
cycD1/CCND1↝,
EGFR↝,
IL6↝,
β-catenin/ZEB1↝,
mTOR↝,
NRF2↝,
AP-1↝,
Cyt‑c↝,
PI3K↝,
PTEN↝,
Cyc↝,
TNF-α↝,

989- EGCG,  Citrate,    In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity
- in-vitro, HCC, NA - in-vivo, NA, NA
PFK↓,
Glycolysis↓, only inhibited glycolysis in cancer cells with a high rate of aerobic glycolysis (HCC-LM3 and HepG2 cells) but not in low-glycolytic cells (Huh-7 and LO2 cells).
lactateProd↓,
GlucoseCon↓,
TumCP↓,
TumCCA↑, arrests cells in S Phage
Casp3↑, citrate enhanced the EGCG upregulation of active caspase-3 and cleaved-PARP in both HCC-LM3 and HepG2 cells
cl‑PARP↑,
Apoptosis↑,
Casp8↑,
Casp9↑,
Cyt‑c↝, translocation of cytochrome c from the mitochondria into the cytosol
MMP↓,
BAD↑,
GLUT2↓, figure2 c,d
PKM2∅, figure2 c,d

2545- M-Blu,    Reversing the Warburg Effect as a Treatment for Glioblastoma
- in-vitro, GBM, U87MG - NA, AD, NA - in-vitro, GBM, A172 - in-vitro, GBM, T98G
Warburg↓, Here, we documented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen consumption and reduction of lactate production in GBM cell lines
OCR↑, increases cellular oxygen consumption, and decreases lactate production in murine hippocampal cells
lactateProd↓,
TumCP↓, MB decreases GBM cell proliferation and halts the cell cycle in S phase.
TumCCA↑,
AMPK↑, Through activation of AMP-activated protein kinase, MB inactivates downstream acetyl-CoA carboxylase and decreases cyclin expression.
ACC↓,
Cyc↓,
neuroP↑, There is mounting evidence that MB enhances brain metabolism and exerts neuroprotective effects in multiple neurodegenerative disease models including Parkinson, Alzheimer, and Huntington disease
Cyt‑c↝, MB has long been known as an electron carrier, which is best represented by MB ability to increase the rate of cytochrome c reduction in isolated mitochondria
Glycolysis↓, MB Decreases Aerobic Glycolysis in U87 Cells
ECAR↓, MB increases OCR and decreases ECAR in U87 cells
TumCG↓, MB Inhibits Tumor Growth in Vitro
other↓, MB dramatically inhibits expression of cyclin A2, B1,and D1 while having less effect on cyclin E1

2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, PEMFs act on the cell, it will firstly change the cell membrane transport capacity, osmotic potential and ionic valves
p‑ERK↝, Also, it will cause changes in mitochondrial protein profile, decrease mitochondrial phosphor-ERK (extracellular-signal-regulated kinase), p53, and cytochrome c, and activate OxPhos.
P53↝,
Cyt‑c↝,
OXPHOS↑,
Apoptosis↑, PEMFs decreases cellular stress factors, increase energy demand, this series of reactions will eventually lead to apoptosis.
ROS↑, The introduction of PEFs and PEMFs can improve the penetration efficiency of ROS, not only reduce the concentration of drugs, but also reduce the irradiation dose of CAP, w

2028- PB,    Potential of Phenylbutyrate as Adjuvant Chemotherapy: An Overview of Cellular and Molecular Anticancer Mechanisms
- Review, Var, NA
HDAC↓, Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).
TumCCA↑, phenylbutyrate treatment that results in reduced proliferation and cell-cycle arrest in G1 or G2 phases.
P21↑, common sequela of phenylbutyrate treatment is the upregulation of p21,
Dose↝, In prostate cancer, phenylbutyrate at clinically achievable concentrations (0.1 mM-8 mM),
Telomerase↓, butyrate or its derivatives was also evident in several other types of cancers and was associated with loss of telomerase activity
IGFBP3↑, Upregulation of insulin-like growth factor binding protein 3 (IGFBP-3) is another unique antiproliferative mechanism of sodium butyrate in breast cancer cells
p‑p38↑, Phenylbutyrate and its derivatives upregulated p21, gelsolin, phosphorylated p38, JNK, and ERK (MAPK pathway members), Bax, caspases-3,
JNK↑,
ERK↑,
BAX↑,
Casp3↑,
Bcl-2↓, downregulated Bcl-X L , Bcl-2, cytochrome c, FAK, and survivin
Cyt‑c↝,
FAK↓,
survivin↓,
VEGF↓, Butyrate treatment reduced the level of vascular endothelial growth factor (VEGF)
angioG↓,
DNArepair↓, Inhibition of DNA Repair.
TumMeta↓,
HSP27↑, Moreover, butyrate treatment in colorectal cancer cells resulted in an acute stress response that was associated with HSP27 activation, activation of ASK1 (MAP3K) and p38 MAPK pathway consequently.
ASK1↑,
ROS↑, Also it resulted in elevated cellular levels of reactive oxygen species (ROS) in oral and tongue cancer cells.
eff↑, phenylbutyrate enhanced the cytotoxicity of temozolamide in malignant glioma cells via suppression of the endoplasmic reticulum stress revealed by the decreased expression of GRP78 and GADD153.
ER Stress↓,
GRP78/BiP↓,
CHOP↑, GADD153
AR↓, Sodium butyrate treatment of prostate cancer cells was associated with downregulation of androgen receptor
other?, lots of references in this paper.

4924- PEITC,    Nutri-PEITC Jelly Significantly Improves Progression-Free Survival and Quality of Life in Patients with Advanced Oral and Oropharyngeal Cancer: A Blinded Randomized Placebo-Controlled Trial
- Trial, Oral, NA
QoL↑, higher proportion of participants with improved HRQOL, stable disease, and increased serum p53 levels
P53↑,
OS↑, The PFS time in the study group was significantly longer than that of the control group (p < 0.05).
Cyt‑c↝, Serum cytochrome c levels were non-significantly decreased in the study group
other↝, β-phenylethyl isothiocyanate (PEITC) is a phytochemical naturally present in cruciferous vegetables such as watercress, broccoli, wasabi, and cabbage
ROS↑, PEITC was selectively toxic to numerous types of cancer cells via reactive oxygen species, (ROS)-mediated mechanisms
selectivity↑,
P21↑, PEITC led to increased oxidative stress, nuclear translocation of p53 and p21, and cell cycle arrest in TP53-mutated oral cancer cells
TumCCA↑,
Dose↝, PEITC at 5 or 10 mg per kg body weight can slow down tumor growth and prolong the survival of cancer-bearing mice along with increased p53 expression
BioAv↑, Nutri-PEITC Jelly containing 40 mg of PEITC per day can be absorbed rapidly within a few hours and eliminated completely within 24 h
Weight↑, the Nutri-PEITC Jelly group had a significantly higher proportion of participants with improved BMI than that of the placebo control group (40% vs. 20%, p < 0.05)
chemoP↑, Therefore, Nutri-PEITC Jelly at the dose of 20 mg/day of PEITC did not inhibit the disease progression and the clinical application of this product is rather a functional food for tertiary chemoprevention than a therapy.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↝, 1,   OXPHOS↑, 1,   ROS↑, 3,   ROS↝, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   AMPK↑, 1,   ECAR↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 2,   lactateProd↓, 2,   PFK↓, 1,   PKM2∅, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↝, 1,   Apoptosis↑, 3,   Apoptosis↝, 1,   ASK1↑, 1,   BAD↑, 1,   BAX↑, 1,   BAX↝, 2,   Bcl-2↓, 1,   Bcl-2↝, 2,   Bcl-xL↝, 1,   Casp3↑, 2,   Casp3↝, 2,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↝, 7,   JNK↑, 1,   JNK↝, 1,   p‑p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

other?, 1,   other↓, 1,   other↝, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   HSP27↑, 1,  

DNA Damage & Repair ⓘ

DNArepair↓, 1,   P53↑, 1,   P53↝, 2,   PARP↝, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

Cyc↓, 1,   Cyc↝, 1,   cycD1/CCND1↝, 2,   P21↑, 2,   P21↝, 2,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   p‑ERK↝, 1,   HDAC↓, 1,   IGFBP3↑, 1,   mTOR↝, 1,   PI3K↝, 1,   PTEN↝, 1,   TumCG↓, 1,  

Migration ⓘ

AP-1↝, 1,   FAK↓, 1,   MMP2↝, 1,   p44↓, 1,   TumCP↓, 3,   TumMeta↓, 1,   β-catenin/ZEB1↝, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   EGFR↝, 1,   VEGF↓, 1,   VEGF↝, 1,   p‑VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↝, 2,   IL6↝, 1,   NF-kB↓, 1,   NF-kB↝, 1,   PSA↝, 1,   TNF-α↝, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   AR↝, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Dose↝, 2,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   AR↝, 1,   EGFR↓, 1,   EGFR↝, 1,   IL6↝, 1,   PSA↝, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   neuroP↑, 1,   OS↑, 1,   QoL↑, 1,   Weight↑, 1,  
Total Targets: 99

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
1 Bufalin/Huachansu
1 Curcumin
1 Ursolic acid
1 EGCG (Epigallocatechin Gallate)
1 Citric Acid
1 Methylene blue
1 Magnetic Fields
1 Phenylbutyrate
1 Phenethyl isothiocyanate
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

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