RECK Cancer Research Results

RECK, Reversion Inducing Cysteine-Rich Protein with Kazal Motifs: Click to Expand ⟱
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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↑,

6388- Eug,    Eugenol’s anti-cancer properties, its modulation of signalling pathways, and cascades across various cancers: A review
- Review, Var, NA
Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3 protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,   Thiols↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis?, 1,   Apoptosis↑, 1,   BAD↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 1,   Cyt‑c↝, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   HATs↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   E2Fs↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   EpCAM↓, 1,   FOXO3↝, 1,   mTOR↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 2,   RECK↑, 3,   TIMP1↑, 1,   TIMP2↑, 2,   TumCI↓, 2,   TumMeta↓, 2,   VEGFR1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IκB↑, 1,   NF-kB↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   IL6↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   antiNeop↑, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   neuroP↑, 1,   Pain↓, 1,   toxicity↝, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 21

Scientific Paper Hit Count for: RECK, Reversion Inducing Cysteine-Rich Protein with Kazal Motifs
2 Eugenol
1 EGCG (Epigallocatechin Gallate)
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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