SIRT6 Cancer Research Results

SIRT6, Sirtuin 6: Click to Expand ⟱
Source:
Type:
– SIRT6 is involved in maintaining genomic stability through its roles in DNA repair and chromatin remodeling.
– By promoting efficient DNA repair, SIRT6 may help prevent the accumulation of genetic mutations that drive tumorigenesis.

– In several studies, lower SIRT6 expression has been associated with more aggressive tumor behavior and poorer overall survival, supporting its role as a tumor suppressor in those contexts.
– Conversely, in some cancers, higher SIRT6 expression has been linked to enhanced survival signaling or metabolic reprogramming that might support tumor growth, suggesting a possible oncogenic role.
Scientific Papers found: Click to Expand⟱
7907- Api,  IVT,    Anticancer Potential of Apigenin and Isovitexin with Focus on Oncogenic Metabolism in Cancer Stem Cells
- Review, Var, NA
ChemoSen↑, Two natural flavonoids, apigenin and isovitexin, have been shown to act synergistically with conventional chemotherapeutic drugs by sensitizing CSCs, ultimately leading to improved therapeutic efficacy.
CSCs↓,
Wnt↓, suppression of the Wnt/β-catenin signaling pathway, the inhibition of nuclear factor-κB protein expression, and the downregulation of the cell cycle via upregulation of p21 and cyclin-dependent kinases
β-catenin/ZEB1↓,
PI3K↓, Figure 3
MMP↓,
TumMeta↓,
MAPK↓,
VEGF↓,
MMP9↓,
TGF-β↓,
Inflam↓,
COX2/PTGS2↓,
IL6↓,
NF-kB↓,
TumCCA↑,
P53↑,
cycD1/CCND1↓,
BAX↑,
Casp↓,
Bcl-2↓,
CD133↓, Brain U87MG and U373MG Apigenin 25–50 μM for 2–21 days ↓Self-renewal capacity, ↓cell growth, ↓clonogenicity, ↓invasiveness ↓CD133, ↓NANOG, ↓SOX2, ↓c-Met, ↓Akt
Nanog↓,
SOX2↓,
Akt↓,
TumCP↓, Breast MDA-MB-231 and MDA-MB-436 Apigenin 2–64 μM for 48 h ↓Proliferation, ↓migration, ↓stemness features, ↓mammospheres, ↓self-renewal capability ↓YAP/TAZ activity, ↓CTGF, ↓CYR61, ↓YAP/TAZ-TEADs
TumCMig↓,
YAP/TEAD↓,
CCN2/CTGF↓,
CCN1/CYR61↓,
SIRT3↓, Breast TNBCs Apigenin 12.5–200 µg/µL for 24 h ↓Stemness properties, ↓mammosphere formation, ↓clonogenic potential ↓SIRT3, ↓SIRT6
SIRT6↓,
PCNA↓, Osteosarcoma U2OS-SC tumors in nude mice Isovitexin 10–40 mg/kg for 2 weeks ↓Tumor growth, ↓tumor size ↓CD133, ↓PCNA, ↓Bcl-2, ↓ DNMT1, ↑apoptotic index, ↑miR-34a
DNMT1↓,
miR-34a↑,

1547- Api,    Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading
- Review, NA, NA
angioG↓,
EMT↓,
CSCs↓,
TumCCA↑,
Dose∅, Dried parsley 45,035ug/g: Dried chamomille flower 3000–5000ug/g: Parsley 2154.6ug/g:
ROS↑, activity of Apigenin has been linked to the induction of oxidative stress in cancer cells
MMP↓, triggering intracellular ROS accumulation and loss of mitochondrial integrity
Catalase↓, catalase and glutathione (GSH), molecules involved in alleviating oxidative stress, were downregulated after Apigenin
GSH↓,
PI3K↓, suppression of the PI3K/Akt and NF-κB
Akt↓,
NF-kB↓,
OCT4↓, glycosylated form of Apigenin (i.e., Vitexin) was able to suppress stemness features of human endometrial cancer, as documented by the downregulation of Oct4 and Nanog
Nanog↓,
SIRT3↓, inhibition of sirtuin-3 (SIRT3) and sirtuin-6 (SIRT6) protein levels
SIRT6↓,
eff↑, ability of Apigenin to interfere with CSC features is often enhanced by the co-administration of other flavonoids, such as chrysin
eff↑, Apigenin combined with a chemotherapy agent, temozolomide (TMZ), was used on glioblastoma cells and showed better performance in cell arrest at the G2 phase compared with Apigenin or TMZ alone,
Cyt‑c↑, release of cytochrome c (Cyt c)
Bax:Bcl2↑, Apigenin has been shown to induce the apoptosis death pathway by increasing the Bax/Bcl-2 ratio
p‑GSK‐3β↓, Apigenin has been shown to prevent activation of phosphorylation of glycogen synthase kinase-3 beta (GSK-3β)
FOXO3↑, Apigenin administration increased the expression of forkhead box O3 (FOXO3)
p‑STAT3↓, Apigenin can induce apoptosis via inhibition of STAT3 phosphorylation
MMP2↓, downregulation of the expression of MMP-2 and MMP-9
MMP9↓,
COX2/PTGS2↓, downregulation of PI3K/Akt in leukemia HL60 cells [156,157] and of COX2, iNOS, and reactive oxygen species (ROS) accumulation in breast cancer cells
MMPs↓, triggering intracellular ROS accumulation and loss of mitochondrial integrity, as proved by low MMP in Apigenin-treated cells
NRF2↓, suppressed the nuclear factor erythroid 2-related factor 2 (Nrf2)
HDAC↓, inhibition of histone deacetylases (HDACs) is the mechanism through which Apigenin induces apoptosis in prostate cancer cells
Telomerase↓, Apigenin has been shown to downregulate telomerase activity
eff↑, Indeed, co-administration with 5-fluorouracil (5-FU) increased the efficacy of Apigenin in human colon cancer through p53 upregulation and ROS accumulation
eff↑, Apigenin synergistically enhances the cytotoxic effects of Sorafenib
eff↑, pretreatment of pancreatic BxPC-3 cells for 24 h with a low concentration of Apigenin and gemcitabine caused the inhibition of the GSK-3β/NF-κB signaling pathway, leading to the induction of apoptosis
eff↑, In NSCLC cells, compared to monotherapy, co-treatment with Apigenin and naringenin increased the apoptotic rate through ROS accumulation, Bax/Bcl-2 increase, caspase-3 activation, and mitochondrial dysfunction
eff↑, Several studies have shown that Apigenin-induced autophagy may play a pro-survival role in cancer therapy; in fact, inhibition of autophagy has been shown to exacerbate the toxicity of Apigenin
XIAP↓,
survivin↓,
CK2↓,
HSP90↓,
Hif1a↓,
FAK↓,
EMT↓,

6342- DRE,    Mechanistic Study on the Inhibitory Effect of Dandelion Extract on Breast Cancer Cell Proliferation and Its Induction of Apoptosis
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
eff↑, MTT assays revealed that the ethyl acetate fraction exhibited the strongest inhibitory effect on cell proliferation.
selectivity↑, 12 potential active compounds, including sesquiterpenes such as Isoalantolactone and Artemisinin, which showed significantly lower toxicity toward normal mammary epithelial MCF-10A cells compared to tumor cells (
Apoptosis↑, the extract induced apoptosis in a dose-dependent manner, with an apoptosis rate as high as 85.04%, and significantly arrested the cell cycle at the S and G2/M phases
TumCCA↑,
PI3K↓, antitumor effects were primarily mediated through the regulation of PI3K-Akt (hsa04151), JAK-STAT (hsa04630), and PPAR (hsa03320) signaling pathways.
Akt↓, these active compounds exhibited strong binding affinities with key target proteins such as PI3K and JAK1
JAK1↓,
STAT↓,
PPARγ↑, EA-2 may remodel tumor cell lipid metabolism by activating the PPARγ pathway
TumCP↓, EA-2 Inhibits the Proliferation of MDA-MB-231 Breast Cancer Cells In Vitro
SIRT6↓, PI3K, AKT1S1, SIRT6, JAK1, SCD, STAT3, CASP8, STAT6, PAK1, and FABP4—were significantly downregulated.
SCD1↓,
STAT3↓,
Casp8↓,
STAT6↓,
PAK1↓,
FABP4↓,

7871- isoO,  Cisplatin,    Isoorientin reverses lung cancer drug resistance by promoting ferroptosis via the SIRT6/Nrf2/GPX4 signaling pathway
- vitro+vivo, Lung, NA
ChemoSen↑, combination of isoorientin (IO) and DDP treatment resulted in a significant decrease in the viability of drug-resistant cells, a substantial increase in intracellular iron, malondialdehyde (MDA) and ROS concentrations
i-Iron↑,
i-MDA↑,
*i-ROS↑,
GSH↓, a notable decrease in glutathione concentration, and the occurrence of ferroptosis in cells, as revealed by in vitro and in vivo experiments.
Ferroptosis↑,
NRF2↓, there was a decrease in the expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2), glutathione peroxidase 4 (GPX4), and sirtuin 6 (SIRT6) proteins, and an increase in cellular ferroptosis.
GPx4↓,
SIRT6↓,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CCN1/CYR61↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 2,   i-Iron↑, 1,   i-MDA↑, 1,   NRF2↓, 2,   ROS↑, 1,   SIRT3↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FABP4↓, 1,   PPARγ↑, 1,   SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp↓, 1,   Casp8↓, 1,   CK2↓, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   MAPK↓, 1,   survivin↓, 1,   Telomerase↓, 1,   YAP/TEAD↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP90↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1,   P53↑, 1,   PCNA↓, 1,   SIRT6↓, 4,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD133↓, 1,   CSCs↓, 2,   EMT↓, 2,   FOXO3↑, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 1,   miR-34a↑, 1,   Nanog↓, 2,   OCT4↓, 1,   PI3K↓, 3,   SOX2↓, 1,   STAT↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   STAT6↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

CCN2/CTGF↓, 1,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 2,   MMPs↓, 1,   PAK1↓, 1,   TGF-β↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   IL6↓, 1,   Inflam↓, 1,   JAK1↓, 1,   NF-kB↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   Dose∅, 1,   eff↑, 8,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  
Total Targets: 76

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

i-ROS↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: SIRT6, Sirtuin 6
2 Apigenin (mainly Parsley)
1 Isovitexin
1 Dandelion Root
1 isoorientin
1 Cisplatin
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#:1135  State#:%  Dir#:1
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