TumCCA Cancer Research Results

TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.
Scientific Papers found: Click to Expand⟱
1450- Bos,  Cisplatin,    3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells
- in-vitro, Pca, DU145
ROS↑, increased reactive oxygen species (ROS) generation
MMP↓,
Casp↑,
Apoptosis↑,
Bax:Bcl2↑,
TumCCA?, induce G0/G1 arrest
cycD1/CCND1↓,
CDK4↓,
P21↑,
p27↑,
NOTCH↓, AKBA demonstrated significant downregulation of Notch signaling mediators
ChemoSen↑, AKBA has the potential to synergistically enhance the cytotoxic efficacy of cisplatin

5767- CAPE,    Caffeic Acid Phenethyl Ester Is a Potential Therapeutic Agent for Oral Cancer
- Review, Oral, NA
TumCP↓, CAPE treatment can effectively suppress the proliferation, survival, and metastasis of oral cancer cells.
tumCV↓,
TumMeta↓,
Akt↓, CAPE treatment inhibits Akt signaling, cell cycle regulatory proteins, NF-κB function, as well as activity of matrix metalloproteinase (MMPs), epidermal growth factor receptor (EGFR), and Cyclooxygenase-2 (COX-2).
NF-kB↓,
MMPs↓,
EGFR↓,
COX2↓,
TumCCA?, CAPE treatment induces cell cycle arrest and apoptosis in oral cancer cells.

3236- EGCG,  Buty,    Molecular mechanisms for inhibition of colon cancer cells by combined epigenetic-modulating epigallocatechin gallate and sodium butyrate
- in-vitro, Colon, RKO - in-vitro, Colon, HCT116 - in-vitro, Colon, HT29
Apoptosis↑, combination treatment induced apoptosis and cell cycle arrest in RKO, HCT-116 and HT-29 colorectal cancer cells.
TumCCA?,
HDAC1↓, decrease in HDAC1, DNMT1, survivin and HDAC activity in all three cell lines.
DNMT1↓,
survivin↓,
HDAC↓,
P21↑, induction of p21 and an increase in nuclear factor kappa B (NF-κB)-p65.
NF-kB↑,
γH2AX↑, An increase in double strand breaks as determined by gamma-H2A histone family member X (γ-H2AX) protein levels
ac‑H3↑, induction of histone H3 hyperacetylation was also observed with combination treatment.
DNAdam↑,

1994- PTL,    Parthenolide Inhibits Tumor Cell Growth and Metastasis in Melanoma A2058 Cells
- in-vitro, Melanoma, A2058 - in-vitro, Nor, L929
tumCV↓, PAR significantly reduced the viability of A2058 cancer cells
selectivity?, demonstrating greater potency against cancer cells compared to normal L929 cells (IC50: 20 μM vs. 27 μM after 24h
ROS?, PAR increased ROS production
BAX↑, elevated mRNA expression of pro-apoptotic Bax and NME1 genes
TumCCA?, PAR induced apoptosis and cell cycle arrest in A2058 cells, as evidenced by the increased proportion of cells in the late apoptotic phase and sub-G1 cell cycle arrest
MMP2↓, MMP-2 and MMP-9 mRNA and protein expressions, gelatinase activity, and the migration of A2058 cells were also decreased by PAR
MMP9↓,
TumCMig↓,
eff↑, These results, along with the synergic effect with dacarbazine, indicated that PAR may have the potential to be a therapeutic drug for melanoma by triggering apoptosis and suppressing invasion and migration.

1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, SFN’s role as a natural HDAC-inhibitor is highly relevant
eff↓, SFN exerts stronger anti-proliferative effects on bladder cancer cell lines under hypoxia, compared to normoxic conditions
TumW↓, mice, SFN (52 mg/kg body weight) for 2 weeks reduced tumor weight by 42%
TumW↓, In another study a 63% inhibition was noted when tumor bearing mice were treated with SFN (12 mg/kg body weight) for 5 weeks
angioG↓,
*toxicity↓, In both investigations, the administration of SFN did not evoke apparent toxicity
GutMicro↝, SFN may protect against chemical-induced bladder cancer by normalizing the composition of gut microbiota and repairing pathophysiological destruction of the gut barrier,
AntiCan↑, A prospective study involving nearly 50,000 men indicated that high cruciferous vegetable consumption may reduce bladder cancer risk
ROS↑, Evidence shows that SFN upregulates the ROS level in T24 bladder cancer cells to induce apoptosis
MMP↓,
Cyt‑c↑,
Bax:Bcl2↑,
Casp3↑,
Casp9↑,
Casp8∅,
cl‑PARP↑,
TRAIL↑, ROS generation promotes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity
DR5↑,
eff↓, Blockade of ROS generation inhibited apoptotic activity and prevented Nrf2 activation in cells treated with SFN, pointing to a direct effect of ROS on apoptosis
NRF2↑, SFN potently inhibits carcinogenesis via activation of the Nrf2 pathway
ER Stress↑, endoplasmic reticulum stress evoked by SFN
COX2↓, downregulates COX-2 in T24 cells
EGFR↓, downregulation of both the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2/neu
HER2/EBBR2↓,
ChemoSen↑, gemcitabine/cisplatin and SFN triggered pathway alterations in bladder cancer may open new therapeutic strategies, including a combined treatment regimen to cause additive effects.
NF-kB↓,
TumCCA?, cell cycle at the G2/M phase
p‑Akt↓,
p‑mTOR↓,
p70S6↓,
p19↑, p19 and p21, are elevated under SFN
P21↑,
CD44↓, CD44s expression correlates with induced intracellular levels of ROS in bladder cancer cells variants v3–v7 on bladder cancer cells following SFN exposure
CSCs↓, CD44 is not only involved in cytoskeletal changes and cellular motility but also serves as a cancer stem cell (CSC) marker


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 ⓘ

NRF2↑, 1,   ROS?, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 2,   Casp↑, 1,   Casp3↑, 1,   Casp8∅, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   p27↑, 1,   survivin↓, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   p19↑, 1,   P21↑, 3,   TumCCA?, 5,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   HDAC↓, 2,   HDAC1↓, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   NF-kB↓, 2,   NF-kB↑, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

EGFR↓, 2,   GutMicro↝, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   TumW↓, 2,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
1 Boswellia (frankincense)
1 Cisplatin
1 Caffeic Acid Phenethyl Ester (CAPE)
1 EGCG (Epigallocatechin Gallate)
1 Butyrate
1 Parthenolide
1 Sulforaphane (mainly Broccoli)
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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