DNMT3A Cancer Research Results

DNMT3A, DNA (cytosine-5-)-methyltransferase 3 alpha: Click to Expand ⟱

Source: CGL-Driver Genes

Type: Oncogene

DNA (cytosine-5-)-methyltransferase 3 alpha, commonly referred to as DNMT3A, is an enzyme that plays a crucial role in the process of DNA methylation, which is an important mechanism for regulating gene expression and maintaining genomic stability.
The expression levels of DNMT3A and the presence of mutations can serve as prognostic markers in certain cancers.
In some cancers, DNMT3A is overexpressed, leading to increased DNA methylation of tumor suppressor genes.

Biological Consequences of DNMT3A Loss
-Epigenetic drift rather than uniform hypomethylation
-Persistence of stem-like transcriptional programs
-Increased self-renewal of hematopoietic stem cells
-Impaired differentiation with preserved viability

Importantly, DNMT3A loss does not strongly increase proliferation on its own—it increases clonal persistence and evolutionary potential.

Scientific Papers found: Click to Expand⟱

3435-

aLinA,

Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines

in-vitro,

Cerv,

HeLa

in-vitro,

Cerv,

SiHa

in-vitro,

Cerv,

C33A

DNMTs↓, ALA increased DNA demethylase, HMTs, and HATs while decreasing global DNA methylation, DNMT, HDMs, and HDACs mRNA expression/activity in all cervical cancer cell lines.
HDAC↓,
HATs↑,
hTERT/TERT↓, ALA downregulated hTERT oncogene while upregulating the mRNA expression of TSGs (Tumor Suppressor Genes) CDH1, RARβ, and DAPK in all the cell lines.
CDH1↑,
RARβ↑,
DNMT1↓, In HeLa, ALA treatment reduced DNMT1 mRNA expression by 2.3-fold, 2.9-fold, and 3.3-fold at 20, 40, and 80 μM, respectively,
DNMT3A↓, ALA also reduced DNMT3B mRNA expression: in HeLa by 3.5-fold and 3.2-fold at 40 and 80 μM, i
TET2↑, ALA treatment induced TET2 mRNA expression, with an increase of 3.6-fold in HeLa at 80 μM.
HDAC1↓, ALA treatment in HeLa resulted in a significant reduction in HDAC1 mRNA expression, with decreases of 2.3-fold and 3.8-fold at 40 and 80 μM,
HDAC8↓, Treatment with ALA at 80 μM also led to reductions in HDAC8 mRNA expression by 2.4-fold, 2.0-fold, and 2.0-fold in HeLa, SiHa, and C33A, respectively.
SIRT1↓, ALA additionally decreased SIRT1 mRNA expression in HeLa by 2.4-fold and 2.5-fold at 40 and 80 μM, respectively.
HMTs↑,
EZH2↓, In HeLa, ALA treatment decreased EZH2 mRNA expression by 2.9-fold, 4.2-fold, and 4.2-fold at 20, 40, and 80 µM, respectively.

1561-

Api,

Apigenin Reactivates Nrf2 Anti-oxidative Stress Signaling in Mouse Skin Epidermal JB6 P + Cells Through Epigenetics Modifications

in-vivo,

Nor,

JB6

*NRF2↑, API enhanced the nuclear translocation of Nrf2
*DNMT1↓, API reduced the expression of the DNMT1, DNMT3a, and DNMT3b epigenetic proteins as well as the expression of some HDACs (1–8).
*DNMT3A↓,
*HDAC↓,
*AntiCan↑, results may provide new therapeutic insights into the prevention of skin cancer by dietary phytochemicals.

1433-

Ash,

SFN,

A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

in-vitro,

BC,

MCF-7

1.0 µM WA and 5.0 µM SFN

in-vitro,

BC,

MDA-MB-231

eff↑, synergistic inhibition of cellular viability in MCF-7
Bcl-2↓,
BAX↑,
tumCV↓,
DNMT1↓,
DNMT3A↓, DNMT3A and DNMT3B mRNA expression is down-regulated
HDAC↓, significant decreases in HDAC activity

5179-

BBR,

Regulation of Cell Signaling Pathways by Berberine in Different Cancers: Searching for Missing Pieces of an Incomplete Jig-Saw Puzzle for an Effective Cancer Therapy

Review,

Var,

AMPK↑, Berberine has been shown to potently induce AMP-activated protein kinase (AMPK) in cancer cells
Casp3↑, TRAIL and berberine significantly activated caspase-3 and cleavage of PARP in TRAIL-resistant MDA-MB-468 BCa cells
cl‑PARP↑,
Mcl-1↓, Berberine dose-dependently induced degradation of Mcl-1 and c-FLIP
cFLIP↓,
β-catenin/ZEB1↓, Berberine efficiently inhibited nuclear accumulation of β-catenin.
Wnt↓, berberine to inhibit the WNT pathway in different cancers
STAT3↓, Berberine reduced protein levels of STAT3
mTOR↓, berberine has anti-tumor effects, through inhibition of the mTOR-signaling pathway.
Hif1a↓, HIF-1α protein expression, a well-known transcription factor critical for dysregulated cancer cell glucose metabolism, was considerably inhibited in berberine-treated colon cancer cell
NF-kB↓, Berberine also interfered with the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway and effectively inhibited colon cancer progression
SIRT1↑, Berberine was shown to upregulate some histone deacetylases (HDAC) of class II, such as sirtuin SIRT1 (sirtuin 1),
DNMT1↓, Berberine induced a decrease in activity of two DNA methylases, DNMT1 (DNA (cytosine-5)-methyltransferase 1) and DNMT3,
DNMT3A↓,
miR-29b↓, Berberine supplementation led to the miR29-b suppression, increasing insulin-like growth factor-binding protein (IGFBP1) expression in the liver;
IGFBP1↑,
eff↑, Silver nanoparticles proved successful in delivering berberine to human tongue squamous carcinoma SCC-25 cells, blocking cell cycle and increasing Bax/Bcl-2 ratio
chemoPv↑, uncovered tremendous chemopreventive ability of berberine to modulate signaling pathways
BioAv↓, Although some issues remain to be solved, such as its poor water solubility/stability and low bioavailability

470-

CUR,

Regulation of carcinogenesis and modulation through Wnt/β-catenin signaling by curcumin in an ovarian cancer cell line

in-vitro,

Ovarian,

SKOV3

20 μM, 96 h

Wnt/(β-catenin)↓,
EMT↓,
DNMT3A↓,
cycD1/CCND1↓,
cMyc↓,
Fibronectin↓,
Vim↓,
E-cadherin↑,
SFRP5↑,

443-

CUR,

Reduced Caudal Type Homeobox 2 (CDX2) Promoter Methylation Is Associated with Curcumin’s Suppressive Effects on Epithelial-Mesenchymal Transition in Colorectal Cancer Cells

in-vitro,

CRC,

SW480

DNMT1↓,
DNMT3A↓,
N-cadherin↓,
Vim↓,
Wnt↓, Wnt3a
Snail↓, Snail1
Twist↓,
β-catenin/ZEB1↓,
E-cadherin↑,
EMT↓, Curcumin incubation inhibited EMT
CDX2↓,

672-

EGCG,

Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer

Review,

NA,

DNMT1↓,
HDAC↓, HDAC1, HDAC2
G9a↓,
PRC2↓,
DNMT3A↓,
67LR↓, anti-proliferative action of EGCG is mediated by the binding to 67LR, whose expression is increased in tumour cells.
Apoptosis↑,
TumCCA↑,

3233-

EGCG,

Epigallocatechin gallate inhibits HeLa cells by modulation of epigenetics and signaling pathways

in-vitro,

Cerv,

HeLa

DNMTs↓, EGCG may competitively inhibit some epigenetic enzymes (DNMT1, DNMT3A, HDAC2, HDAC3, HDAC4, HDAC7 and EZH2).
DNMT1↓,
DNMT3A↓,
HDAC2↓,
HDAC3↓,
HDAC4↓,
EZH2↓, Interaction of EGCG with EZH2 protein indicates inhibition of activity
PI3K↓, Downregulation of key signaling moieties of PI3K, Wnt and MAPK pathways
Wnt↓,
MAPK↓,
hTERT/TERT↓, including TERT, CCNB1, CCNB2, MMP2, MMP7. PIK3C2B, PIK3CA, MAPK8 and IL6 was also observed
MMP2↓,
MMP7↓,
IL6↓,
MDM2↓, Fig 1
MMP-10↓,
TP53↑,
PTEN↑,

4234-

H2,

Hydrogen gas alleviates sepsis-induced neuroinflammation and cognitive impairment through regulation of DNMT1 and DNMT3a-mediated BDNF promoter IV methylation in mice

in-vivo,

Sepsis,

 septic mice.

*cognitive↑, 2% H2 protects against sepsis-induced cognitive impairment in septic mice.
*DNMT1↓, 2% H2 decreases DNMT1, DNMT3a but not DNMT3b levels in the hippocampus.
*DNMT3A↓,
*BDNF↑, 2% H2 enhances BDNF levels through hypomethylating the BDNF promoter IV.

2915-

LT,

Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells

in-vitro,

Colon,

HT29

30 μM

in-vitro,

CRC,

SNU-407

30 μM

in-vitro,

Nor,

FHC

65 μM

DNMTs↓, luteolin inhibited the expression of DNA methyltransferases, a transcription repressor, and increased the expression and activity of ten-eleven translocation (TET) DNA demethylases,
TET1↑,
NRF2↑, luteolin decreased the methylation of the Nrf2 promoter region, which corresponded to the increased mRNA expression of Nrf2
HDAC↓, Recently, Zao et al. demonstrated that luteolin epigenetically activates the Nrf2 pathway by downregulating DNA methyltransferase (DNMT) and histone deacetylase (HDAC) expression
tumCV↓, Luteolin decreased the viability of all three cell lines in a dose-dependent manner
BAX↑, luteolin upregulated the expression of the apoptotic protein Bax, active caspase-9, and active caspase-3, while it downregulated the expression of the anti-apoptotic protein Bcl-2,
Casp9↑,
Casp3↑,
Bcl-2↓,
ROS↓, Luteolin promotes ROS scavenging by inducing the expression of antioxidant enzymes
GSS↑, luteolin increased the protein expression of the antioxidant enzymes GCLc, GSS, catalase, and HO-1 in a dose- and time-dependent manner
Catalase↑,
HO-1↑,
DNMT1↓, Luteolin markedly decreased the protein expression of DNMT1, DNMT3A, and DNMT3B in a dose- and time-dependent manner
DNMT3A↓,
TET1↑, In contrast, it markedly increased the protein expression of TET1, TET2, and TET3 in a dose- and time-dependent manner
TET3↑,
TET2↓,
P53↑, Luteolin upregulated the expression of p53 and its target p21 in a dose- and time-dependent manner
P21↑,

3357-

QC,

The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes

in-vitro,

AML,

HL-60

NA,

U937

DNMT1↓, Qu treatment almost eliminates DNMT1 and DNMT3a expression, and this regulation was in part STAT-3 dependent.
DNMT3A↓,
HDAC↓, The treatment also downregulated class I HDACs.
ac‑H3↑, Qu (50 μmol/L) treatment of cell lines for 48 h caused accumulation of acetylated histone 3 and histone 4, resulting in three- to ten fold increases in the promoter region of DAPK1, BCL2L11, BAX, APAF1, BNIP3, and BNIP3L.
ac‑H4↑,
BAX↑,
APAF1↑,
BNIP3↑,
STAT3↑, Quercetin downregulates DNMTs and STAT3

3359-

QC,

Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells

in-vitro,

Cerv,

HeLa

DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
HDAC2↓,
HDAC6↓,
HDAC11↓,
G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
PTEN↑,
SOCS1↑,

3193-

SFN,

Epigenetic Therapeutics Targeting NRF2/KEAP1 Signaling in Cancer Oxidative Stress

Review,

Var,

DNMTs↓, SFN, a natural phytochemical, primarily attenuates both DNMTs and HDACs, individually suppressing DNA hypermethylation and histones deacetylation, ultimately upregulating NRF2.
HDAC↑,
NRF2↑,
DNMT1↓, significant attenuation of DNMT1 and DNMT3a contributed to a decrease in the methylated CpG ratio in the NFE2L2 promoter region in an SFN dose- and time-dependent manner, thus increasing NRF2
DNMT3A↓,
NQO1↑, consequently increasing the transcription of its target genes such as NQO1 and catechol-O-methyltransferase (COMT)
COMT↑,
TumCG↓, SFN may prevent or slow the growth of recurrent prostate cancer, essentially without severe adverse events.
*toxicity↓,

3660-

SFN,

Sulforaphane - role in aging and neurodegeneration

Review,

AD,

*antiOx↑, antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB
*Inflam↓,
*NRF2↑, increased Nrf2 expression and nuclear localization after SFN treatment
*NF-kB↓,
*HDAC↓, inhibiting HDAC and DNA methyltransferases a
*DNMTs↓,
*neuroP↑, prevent neurodegeneration.
*AntiAge↑, “miraculous” drug to prevent aging and neurodegeneration.
*DNMT1↓, decrease the expression of DNA methyltransferases (DNMTs), especially DNMT1 and DNMT3b.
*DNMT3A↓,
*memory↑, SFN prevented the memory impairment induced by OKA in rats.
*HO-1↑, restored Nrf2 and antioxidant protein (GCLC, HO-1) expression
*ROS↓, diminished the oxidative stress by attenuating ROS and NO levels, and increased GSH concentration.
*NO↓,
*GSH↑,
*NF-kB↓, reducing NF-κB and TNF-α, and by rising IL-10
*TNF-α↓,
*IL10↑,

1730-

SFN,

Sulforaphane: An emergent anti-cancer stem cell agent

Review,

Var,

BioAv↓, When exposed to high temperatures during meal preparation, myrosinase can be degraded, lose its function, and subsequently compromise the synthesis of SFN.
BioAv↑, eating raw cruciferous vegetables, instead of heating them can significantly improve the biodisponibility of SFN and its subsequent beneficial effects.
GSTA1↑, induction of Phase II enzymes [glutathione S-transferase (GST)
P450↓, (cytochrome P450, CYP) inhibition
TumCCA↑, herb-derived agent can also promote cell cycle arrest and apoptosis by regulating different signaling pathways including Nuclear Factor erythroid Related Factor 2 (Nrf2)-Keap1 and NF-κB.
HDAC↓, modulate the activity of some epigenetic factors, such as histone deacetylases (HDAC),
P21↑, upregulation of p21 and p27,
p27↑,
DNMT1↓, SFN was able to decrease the expression of DNMT1 and DNMT3 in LnCap prostate cancer cells
DNMT3A↓,
cycD1/CCND1↑, reduce methylation in Cyclin D2 promoter, thus inducing Cyclin D2 gene expression in those cells
DNAdam↑, SFN induced DNA damage, enhanced Bax expression and the release of cytochrome C followed by apoptosis
BAX↑,
Cyt‑c↑,
Apoptosis↑,
ROS↑, SFN increased reactive oxygen species (ROS), apoptosis-inducing factor (AIF)
AIF↑,
CDK1↑,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
NRF2↑, SFN significantly activated the major antioxidant marker Nrf2 and decreased NFκB, TNF-α, IL-1β
NF-kB↓,
TNF-α↓,
IL1β↓,
CSCs↓, SFN, have attracted attention due to their anti-CSC effect
CD133↓,
CD44↓,
ALDH↓,
Nanog↓,
OCT4↓,
hTERT/TERT↓,
MMP2↓,
EMT↓, SFN was reported to inhibit EMT and metastasis in the NSCLC, the cell lines H1299
ALDH1A1↓, ALDH1A1), Wnt3, and Notch4, other CSC-related genes inhibited by SFN treatment
Wnt↓,
NOTCH↓, SFN can inhibit aberrantly activated embryonic pathways in CSCs, including Sonic Hedgehog (SHH), Wnt/β-catenin, Cripto-1 (CR-1), and Notch.
ChemoSen↑, These results suggest that the antioxidant properties of SFN do not impact the cytotoxicity of antineoplastic drugs, but on the contrary, seems to improve it.
*Ki-67↓, Ki-67 and HDAC3 levels significantly decreased in benign breast tissues, and there was also a reduction in HDAC activity in blood cells
*HDAC3↓,
*HDAC↓,

1437-

SFN,

Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition

Review,

NA,

HDAC↓, 15 μM
HDAC1↓,
HDAC2↓,
HDAC3↓,
HDAC8↓,
eff↑, this evidence suggests that sulforaphane may also compromise DNA repair mechanisms in cancer cells with selectivity.
ac‑HSP90↑,
DNMT1↓, 10 μM sulforaphane in 6 days inhibited DNMT1 and DNMT3a expression by 48% and 78%, respectively
DNMT3A↓,
hTERT/TERT↓,
NRF2↑, enhance nuclear translocation of Nrf2 and increase expression of Nrf2-target antioxidant genes, including HO-1, NQO1, and UGT1A1
HO-1↑,
NQO1↑,
miR-155↓,
miR-200c↑,
SOX9↓,
*toxicity↓, broccoli sprout-infused beverage containing 400 μM glucoraphanin nightly for 2 weeks causing no adverse effects and being well tolerated in 200 subjects

3426-

TQ,

Thymoquinone-Induced Reactivation of Tumor Suppressor Genes in Cancer Cells Involves Epigenetic Mechanisms

in-vitro,

BC,

MDA-MB-468

in-vitro,

AML,

24 h with 20 µM of TQ

UHRF1↓, (UHRF1), DNMT1,3A,3B, G9A, HDAC1,4,9, KDM1B, and KMT2A,B,C,D,E, were downregulated in TQ-treated Jurkat cells
DNMT1↓,
DNMT3A↓,
DNMTs↓,
HDAC1↓,
HDAC4↓,
HDAC↓,
DLC1↑, several TSGs, such as DLC1, PPARG, ST7, FOXO6, TET2, CYP1B1, SALL4, and DDIT3, known to be epigenetically silenced in various tumors, including acute leukemia, were upregulated,
PPARγ↑,
FOXO↑,
TET2↑,
CYP1B1↑,
G9a↓, expression of UHRF1, DNMT1, G9a, and HDAC1 genes in both cancer cell (Jurkat cells and MDA-MB-468 cells) lines depends on the TQ dose

3423-

TQ,

Epigenetic role of thymoquinone: impact on cellular mechanism and cancer therapeutics

Review,

Var,

AntiCan↑, Thymoquinone is a natural product with anticancer activity.
Inflam↓, Thymoquinone has been shown to exert anti-inflammatory, antidiabetic, antihypertensive, antimicrobial, analgesic, immunomodulatory, spasmolytic, hepatoprotective, renal-protective, gastroprotective, bronchodilatory, antioxidant and antineoplastic eff
hepatoP↑,
RenoP↑,
BAX↑, Thymoquinone can upregulate proapoptotic genes and proteins, such as Bax/Bak, or downregulate antiapoptotic genes and proteins, such as Bcl-2, Bcl-xL, among others, as well as modulating the caspase pathway
Bak↑,
Bcl-2↓,
Bcl-xL↓,
ROS↑, through the generation of reactive oxygen species (ROS)
P53↑, overexpressed or activated by thymoquinone; for example, p53, PTEN, p21, p27 and breast cancer type 1 susceptibility protein (BRCA1), among others,
PTEN↑,
P21↑,
p27↑,
BRCA1↑,
PI3K↓, (PI3K)/Akt and mitogen-activated protein kinase (MAPK)/ERK, have been found to be inhibited by thymoquinone
Akt↓,
MAPK↓,
ERK↓,
p‑ERK↓, thymoquinone reduces ERK phosphorylation and matrix metalloproteinase (MMP) secretion by downregulating focal adhesion kinase (FAK)
MMPs↓,
FAK↓,
Twist↓, downregulates Twist1 and Zeb1 transcription factors, and thus inhibits epithelial to mesenchymal transition (EMT) and subsequently inhibits cancer metastasis
Zeb1↓,
EMT↓,
TumMeta↓,
angioG↓, thymoquinone can inhibit angiogenesis by interfering with essential steps of neovascularization, such as suppressing proangiogenic vascular endothelial growth factor (VEGF)
VEGF↓,
HDAC↓, HDACs are usually overexpressed in MCF-7 breast cancer cells, and thymoquinone can act as a HDAC inhibitor (HDACi) that potently induces apoptosis through inducing acetylation of histones and inhibiting deacetylation of histones.
Maspin↑, thymoquinone reactivates HDAC target genes (p21 and Maspin), inducing the upregulation of Bax
SIRT1↑, thymoquinone can upregulate SIRT1 expression in neonatal rat cardiomyocytes and consequently deacetylates p53; thus, it can act as an apoptosis inducer
DNMT1↓, Collectively, they suggested that thymoquinone induces methylation of DNA via binding with DNMT1 and suppressing its expression,
DNMT3A↓, thymoquinone decreases the expression of some important epigenetic proteins like DNMT1,3A,3B, G9A, HDAC1,4,9, KDM1B, KMT2A,B,C,D,E and UHRF1 in Jurkat cells,
HDAC1↓,
HDAC4↓,

Showing Research Papers: 1 to 18 of 18

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, GSH↑, 1, HO-1↑, 1, NRF2↑, 2, ROS↓, 1,

DNA Damage & Repair ⓘ

DNMT1↓, 3, DNMT3A↓, 3, DNMTs↓, 1,

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 3, HDAC3↓, 1,

Migration ⓘ

Ki-67↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1,

Immune & Inflammatory Signaling ⓘ

IL10↑, 1, Inflam↓, 1, NF-kB↓, 2, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,

Clinical Biomarkers ⓘ

Ki-67↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 1, cognitive↑, 1, memory↑, 1, neuroP↑, 1, toxicity↓, 2,
Total Targets: 24

Scientific Paper Hit Count for: DNMT3A, DNA (cytosine-5-)-methyltransferase 3 alpha

5 Sulforaphane (mainly Broccoli)
2 Curcumin
2 EGCG (Epigallocatechin Gallate)
2 Quercetin
2 Thymoquinone
1 alpha Linolenic acid
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Berberine
1 Hydrogen Gas
1 Luteolin

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#:86  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

DNMT3A Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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