SIRT2 Cancer Research Results

SIRT2, Sirtuin 2: Click to Expand ⟱
Source:
Type:
SIRT2 is primarily localized in the cytoplasm but can also shuttle into the nucleus, where it regulates multiple cellular functions.
It deacetylates various substrates including histones and non-histone proteins, thereby influencing gene expression, cell cycle progression, and cytoskeletal dynamics.
SIRT2’s enzymatic activity is dependent on NAD⁺ levels, linking its function to the metabolic state of the cell.

Lower expression levels often correlate with more aggressive disease and poorer prognosis in certain contexts, although some studies suggest that overexpression can also be deleterious in specific settings.
Scientific Papers found: Click to Expand⟱
5905- CAR,  HCQ,    Synergistic inhibition of metastatic melanoma by carvacrol and chloroquine: an in vitro and in silico investigation of apoptosis and molecular targets
- in-vitro, Melanoma, NA
eff↑, While carvacrol monotherapy exhibited weak cytotoxicity, its combination with non-toxic concentrations of chloroquine resulted in a potent and synergistic reduction in WM9 cell viability
tumCV↑,
IGF-1R↓, both carvacrol and chloroquine bind with high affinity to common molecular targets, including Insulin-Like Growth Factor 1 Receptor and Sirtuin-2.
SIRT2↓, CV and CQ may function as novel SIRT2 inhibitors
HSP90↓, Finally, our analysis confirmed that CQ, but not CV, strongly interacts with HSP90, a key chaperone protein that is frequently overexpressed in cancer
TumCP↓, Crucially, combining the two agents produced a powerful antiproliferative effect.
Akt↓, carvacrol has been shown to inhibit Akt activation in other cancer types [

2687- RES,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, NA, NA - Review, AD, NA
NF-kB↓, RES affects NF-kappaB activity and inhibits cytochrome P450 isoenzyme (CYP A1) drug metabolism and cyclooxygenase activity.
P450↓,
COX2↓,
Hif1a↓, RES may inhibit also the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) and thus may have anti-cancer properties
VEGF↓,
*SIRT1↑, RES induces sirtuins, a class of proteins involved in regulation of gene expression. RES is also considered to be a SIRT1-activating compound (STACs).
SIRT1↓, In contrast, decreased levels of SIRT1 and SIRT2 were observed after treatment of BJ cells with concentrations of RES
SIRT2↓,
ChemoSen⇅, However, the effects of RES remain controversial as it has been reported to increase as well as decrease the effects of chemotherapy.
cardioP↑, RES has been shown to protect against doxorubicin-induced cardiotoxicity via restoration of SIRT1
*memory↑, RES has been shown to inhibit memory loss and mood dysfunction which can occur during aging.
*angioG↑, RES supplementation resulted in improved learning in the rats. This has been associated with increased angiogenesis and decreased astrocytic hypertrophy and decreased microglial activation in the hippocampus.
*neuroP↑, RES may have neuroprotective roles in AD and may improve memory function in dementia.
STAT3↓, RES was determined to inhibit STAT3, induce apoptosis, suppress the stemness gene signature and induced differentiation.
CSCs↓,
RadioS↑, synergistically increased radiosensitivity. RES treatment suppressed repair of radiation-induced DNA damage
Nestin↓, RES decreased NESTIN
Nanog↓, RES was determined to suppress the expression of NANOG
TP53↑, RES treatment activated TP53 and p21Cip1.
P21↑,
CXCR4↓, RES downregulated nuclear localization and activity of NF-kappa-B which resulted in decreased expression of MMP9 and C-X-C chemokine receptor type 4 (CXCR4), two proteins associated with metastasis.
*BioAv↓, The pharmacological properties of RES can be enhanced by nanoencapsulation. Normally the solubility and stability of RES is poor.
EMT↓, RES was determined to suppress many gene products associated with EMT such as decreased vimentin and SLUG expression but increased E-cadherin expression.
Vim↓,
Slug↓,
E-cadherin↑,
AMPK↑, RES can induce AMPK which results in inhibition of the drug transporter MDR1 in oxaliplatin-resistant (L-OHP) HCT116/L-OHP CRCs.
MDR1↓,
DNAdam↑, RES induced double strand DNA breaks by interfering with type II topoisomerase.
TOP2↓, The DNA damage was determined to be due to type II topoisomerase poisoning.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt.
Akt↓,
Wnt↓, RES was shown to decrease WNT/beta-catenin pathway activity and the downstream targets c-Myc and MMP-7 in CRC cells.
β-catenin/ZEB1↓,
cMyc↓,
MMP7↓,
MALAT1↓, RES also decreased the expression of long non-coding metastasis associated lung adenocarcinoma transcript 1 (RNA-MALAT1) in the LoVo and HCT116 CRC cells.
TCF↓, Treatment of CRC cells with RES resulted in decreased expression of transcription factor 4 (TCF4), which is a critical effector molecule of the WNT/beta-catenin pathway.
ALDH↓, RES was determined to downregulate ALDH1 and CD44 in HNC-TICs in a dose-dependent fashion.
CD44↓,
Shh↓, RES has been determined to decrease IL-6-induced Sonic hedgehog homolog (SHH) signaling in AML.
IL6↓, RES has been shown to inhibit the secretion of IL-6 and VEGF from A549 lung cancer cells
VEGF↓,
eff↑, Combined RES and MET treatment resulted in a synergistic response in terms of decreased TP53, gammaH2AX and P-Chk2 expression. Thus, the combination of RES and MET might suppress some of the aging effects elicited by UVC-induced DNA damage
HK2↓, RES treatment resulted in a decrease in HK2 and increased mitochondrial-induced apoptosis.
ROS↑, RES was determined to shut off the metabolic shift and increase ROS levels and depolarized mitochondrial membranes.
MMP↓,


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:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 1,   HK2↓, 1,   SIRT1↓, 1,   SIRT2↓, 2,  

Cell Death ⓘ

Akt↓, 2,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 1,   IGF-1R↓, 1,   Nanog↓, 1,   Nestin↓, 1,   PTEN↑, 1,   Shh↓, 1,   STAT3↓, 1,   TCF↓, 1,   TOP2↓, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MALAT1↓, 1,   MMP7↓, 1,   Slug↓, 1,   TumCP↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   IL6↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen⇅, 1,   eff↑, 2,   MDR1↓, 1,   P450↓, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   TP53↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

SIRT1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 5

Scientific Paper Hit Count for: SIRT2, Sirtuin 2
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#:1289  State#:%  Dir#:1
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