RECK Cancer Research Results

RECK, Reversion Inducing Cysteine-Rich Protein with Kazal Motifs: Click to Expand ⟱
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Type:
RECK (Reversion Inducing Cysteine-Rich Protein with Kazal Motifs) is a protein that has been studied for its role in cancer biology. It is known to function as a tumor suppressor and is involved in the regulation of extracellular matrix remodeling, cell adhesion, and migration.
RECK is generally considered a tumor suppressor. Its expression is often downregulated in various cancers, which can contribute to tumor progression, invasion, and metastasis.
Scientific Papers found: Click to Expand⟱
1503- EGCG,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
selectivity↑, EGCG has been shown to induce apoptosis and cell cycle arrest in many cancer cells without affecting normal cells
DNMT1↓, inhibition of DNMT1 leading to demethylation and reactivation of methylation-silenced genes.
RECK↑, EGCG-induced epigenetic reactivation of RECK
MMPs↓, negatively regulates matrix metalloproteinases (MMPs)
TumCI↓, inhibits tumor invasion, angiogenesis, and metastasis
angioG↓,
TumMeta↓,
HATs↓, EGCG has strong HAT inhibitory activity
IκB↑, increases the level of cytosolic IκBα
NF-kB↓, suppresses tumor necrosis factor α-induced NF-κB activation
IL6↓,
COX2↓,
NOS2↓,
ac‑H3↑, increased the levels of acetylated histone H3 (LysH9/18) and H4 levels
ac‑H4↑,
eff↑, EGCG may synergize with the HDAC inhibitory action of vorinostat to help de-repress silenced tumor suppressor genes regulating key functions such as proliferation and cell survival

6336- Eug,    Eugenol induces apoptosis and inhibits invasion and angiogenesis in a rat model of gastric carcinogenesis induced by MNNG
- in-vivo, GC, NA
Apoptosis?, Rats administered MNNG developed gastric carcinomas that displayed apoptosis avoidance coupled to upregulation of pro-invasive and angiogenic factors
Bcl-2↓, Administration of eugenol induced apoptosis via the mitochondrial pathway by modulating the Bcl-2 family proteins, Apaf-1, cytochrome C, and caspases and inhibiting invasion, and angiogenesis
Cyt‑c↝,
Casp↑,
TumCI↓,
angioG↓,
MMPs↓, as evidenced by changes in the activities of MMPs and the expression of MMP-2 and -9, VEGF, VEGFR1, TIMP-2 and RECK.
VEGF↓,
VEGFR1↓,
TIMP2↑, Administration of eugenol decreased activities of MMPS and the expression of MMP-2, MMP-9, VEGF and VEGFR1 and increased TIMP-2 and RECK expression
RECK↑,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Apoptosis?, 1,   Bcl-2↓, 1,   Casp↑, 1,   Cyt‑c↝, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   HATs↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,  

Migration ⓘ

MMPs↓, 2,   RECK↑, 2,   TIMP2↑, 1,   TumCI↓, 2,   TumMeta↓, 1,   VEGFR1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IκB↑, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   NOS2↓, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: RECK, Reversion Inducing Cysteine-Rich Protein with Kazal Motifs
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:%  Cells:%  prod#:%  Target#:271  State#:%  Dir#:2
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