E2Fs Cancer Research Results

E2Fs, E2F family of transcription factors: Click to Expand ⟱

Source: HalifaxProj(inactivate)

Type:

E2Fs have been classified as transcriptional activators (E2F1-3) or transcriptional repressors (E2F4-8), and are thus predicted to play a dual role in human cancers.
Activators: E2F1,2,3a,3b
Repressors: E2F4,5,6,7a,7b,8
As a tumor suppressor and oncogene, the transcription factor E2F1 is a downstream regulator of the Rb pathway.
The role of E2Fs in CSCs is widely regarded as an activator gene. Up-regulation of E2Fs is reported to be involved in proliferation promotion (21), maintenance and acquisition of self-renewal (22, 23), invasion and metastatic progression (24) and resistance to chemotherapy and radiotherapy (25) in many CSCs.

Scientific Papers found: Click to Expand⟱

1552-

Api,

Apigenin inhibits the growth of colorectal cancer through down-regulation of E2F1/3 by miRNA-215-5p

in-vitro,

CRC,

HCT116

Apoptosis↑,
TumCP↓,
miR-215-5p↑, miRNA-215-5p showed markedly increased
TumCCA↑, cell cycle arrest at G0/G1 phase induced by API
E2Fs↓, down-regulation of E2F1/3 by miRNA-215-5p

3391-

ART/DHA,

Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug

Review,

Var,

TumCP↓, inhibiting cancer proliferation, metastasis, and angiogenesis.
TumMeta↓,
angioG↓,
TumVol↓, reduces tumor volume and progression
BioAv↓, artemisinin has low solubility in water or oil, poor bioavailability, and a short half-life in vivo (~2.5 h)
Half-Life↓,
BioAv↑, semisynthetic derivatives of artemisinin such as artesunate, arteeter, artemether, and artemisone have been effectively used as antimalarials with good clinical efficacy and tolerability
eff↑, preloading of cancer cells with iron or iron-saturated holotransferrin (diferric transferrin) triggers artemisinin cytotoxicity
eff↓, Similarly, treatment with desferroxamine (DFO), an iron chelator, renders compounds inactive
ROS↑, ROS generation may contribute with the selective action of artemisinin on cancer cells.
selectivity↑, Tumor cells have enhanced vulnerability to ROS damage as they exhibit lower expression of antioxidant enzymes such as superoxide dismutase, catalase, and gluthatione peroxidase compared to that of normal cells
TumCCA↑, G2/M, decreased survivin
survivin↓,
BAX↑, Increased Bax, activation of caspase 3,8,9 Decreased Bc12, Cdc25B, cyclin B1, NF-κB
Casp3↓,
Casp8↑,
Casp9↑,
CDC25↓,
CycB/CCNB1↓,
NF-kB↓,
cycD1/CCND1↓, decreased cyclin D, E, CDK2-4, E2F1 Increased Cip 1/p21, Kip 1/p27
cycE/CCNE↓,
E2Fs↓,
P21↑,
p27↑,
ADP:ATP↑, Increased poly ADP-ribose polymerase Decreased MDM2
MDM2↓,
VEGF↓, Decreased VEGF
IL8↓, Decreased NF-κB DNA binding [74, 76] IL-8, COX2, MMP9
COX2↓,
MMP9↓,
ER Stress↓, ER stress, degradation of c-MYC
cMyc↓,
GRP78/BiP↑, Increased GRP78
DNAdam↑, DNA damage
AP-1↓, Decreased NF-κB, AP-1, Decreased activation of MMP2, MMP9, Decreased PKC α/Raf/ERK and JNK
MMP2↓,
PKCδ↓,
Raf↓,
ERK↓,
JNK↓,
PCNA↓, G2, decreased PCNA, cyclin B1, D1, E1 [82] CDK2-4, E2F1, DNA-PK, DNA-topo1, JNK VEGF
CDK2↓,
CDK4↓,
TOP2↓, Inhibition of topoisomerase II a
uPA↓, Decreased MMP2, transactivation of AP-1 [56, 88] NF-κB uPA promoter [88] MMP7
MMP7↓,
TIMP2↑, Increased TIMP2, Cdc42, E cadherin
Cdc42↑,
E-cadherin↑,

6340-

Eug,

Eugenol triggers apoptosis in breast cancer cells through E2F1/survivin down-regulation

in-vitro,

BC,

MCF-7

in-vitro,

BC,

T47D

in-vitro,

BC,

MDA-MB-231

tumCV↓, Eugenol at low dose (2 μM) has specific toxicity against different breast cancer cells.
E2Fs↓, strong down-regulation of E2F1 and its downstream antiapoptosis target survivin, independently of the status of p53 and ERα.
survivin↓,
NF-kB↓, Eugenol inhibited also several other breast cancer related oncogenes, such as NF-κB and cyclin D1
cycD1/CCND1↓,
P21↑, eugenol up-regulated the versatile cyclin-dependent kinase inhibitor p21WAF1 protein, and inhibited the proliferation of breast cancer cells in a p53-independent manner.
TumCP↓,
Apoptosis↑, eugenol induced apoptosis and inhibited invasion and angiogenesis in a rat model of gastric carcinogenesis
TumCI↓,
angioG↓,

6325-

Eug,

Anticancer Properties of Eugenol: A Review

Review,

Var,

*antiOx↑, long been utilized all over the world as a result of its broad properties like antioxidant, anticancer, anti-inflammatory, and antimicrobial activities. Both eugenol and clove oil display potent antioxidant capabilities.
*AntiCan↑,
*Inflam↓, Eugenol Anti-Inflammatory Agent
TumCD↑, Anticancer effects of eugenol are accomplished by various mechanisms like inducing cell death, cell cycle arrest, inhibition of migration, metastasis, and angiogenesis on several cancer cell lines.
TumCCA↑,
TumCMig↓,
TumMeta↓,
angioG↓,
ChemoSen↑, eugenol might be utilized as an adjunct remedy for patients who are treated with conventional chemotherapy. This combination leads to a boosted effectiveness with decreased toxicity.
chemoP↑,
*BioAv↝, Eugenol is an aromatic pale yellowish liquid that dissolves well in organic solvents and moderately in water.
*BioAv↑, Eugenol is susceptible to oxidation and many biochemical interactions. It is quickly absorbed via diverse organs and processed in the liver when taken orally.
*BioAv↑, encapsulation of eugenol appears to be the finest approach for avoiding early absorption, improving its water solubility, and, therefore, increasing its action.
*BioAv↑, when eugenol is supplied as solid lipid nanoparticles, the quantity of eugenol delivered to infected cells upsurges by at least sixfold
*Bacteria↓, Eugenol is well-known for its antibacterial properties.
*ROS↓, They possess a potent DPPH radical scavenging influence (half maximal inhibitory concentration (IC50) = 11.7 μg/mL for eugenol; 13.2 μg/mL for clove oil) and hinder reactive oxygen species (ROS) generation in human neutrophils
*IL6↓, exposure of rats to eugenol (10.7 mg/kg body weight/day) for 15 days reduced the translation of inflammatory markers (IL-6, COX-2, and TNF-α), lipid peroxidation indices, and protein oxidation [51].
*COX2↓,
*TNF-α↓,
*lipid-P↓,
*SOD1↑, Pretreatment with eugenol was capable of dramatically enhancing SOD1, CAT, Gpx1, and GST levels as well as decreasing inflammation triggered via lung exposure to LPS.
*Catalase↑,
*GPx1↑,
*GSTs↑,
ROS↑, Eugenol triggered cell apoptosis in these cancerous cells through a process reliant on elevated ROS production and decreased the mitochondrial membrane potential, indicating that it might possess apoptosis-triggering characteristics
MMP↓,
Apoptosis↑,
COX2↓, Lung cancer in vitro low concentrations to 1000 μM reduces cyclooxygenase-2 activity, promotes cell cycle arrest at S-phase
TumCCA↑,
E2Fs↓, Breast cancer in vitro and in vivo 2 µM down regulating E2F1
PI3K↓, inhibition of the PI3K/Akt pathway and prevention of MMP (matrix metalloproteinase) action, an in-laboratory study using lung cancer
Akt↓,
MMPs↓,
CSCs↓, CSC markers like Oct4, CD44, EpCAM, and Notcht1, whose expression is reliant on β-catenin, were considerably reduced,
OCT4↓,
CD44↓,
EpCAM↓,
NOTCH1↓,
TumVol↓, Eugenol works through the synthesis of ROS [82], which leads to DNA synthesis inhibition, hence postponing cancer progress. A 40% decrease was documented in tumor size via eugenol activity
Casp3↑, Elevated caspase-3, p53, and PARP cleavage levels are associated with eugenol-triggered apoptosis in HOS cells
P53↑,
cl‑PARP↑,
MMP2↓, Eugenol-treated cells demonstrated substantially reduced expression of MMP2 and MMP9 and an insignificant rise in the expression of TIMP1 in HER2-positive and triple-negative breast cancer cells.
MMP9↓,
TIMP1↑,
ALDH↓, Eugenol is thought to help cisplatin suppress breast cancer stem cells by hindering the action of aldehyde dehydrogenases (ALDH) and ALDH-positive cancer beginning cells, as well as inhibiting the NF-B signaling pathway.
NF-kB↓,
*toxicity↓, Overall, the toxic effect of eugenol on mammals is low, and the US Environmental Protection Agency has categorized eugenol as category 3. The oral LD50 value is >1930 mg kg−1 in rodents

6331-

Eug,

Eugenol-Induced Autophagy and Apoptosis in Breast Cancer Cells via PI3K/AKT/FOXO3a Pathway Inhibition

in-vitro,

BC,

MDA-MB-231

Apoptosis↑, Apoptosis was detected by a flow-cytometry technique, while autophagy was detected by acridine orange.
TumAuto↑,
TumCP↓, Treating cells with different concentrations of eugenol significantly inhibited cell proliferation.
Akt↑, The protein levels of AKT serine/threonine kinase 1 (AKT), forkhead box O3 (FOXO3a), cyclin dependent kinase inhibitor 1A (p21), cyclin-dependent kinase inhibitor (p27), and Caspase-3 and -9 increased significantly in Eugenol-treated cells.
FOXO3↑,
P21↑,
p27↑,
Casp3↑,
Casp9↑,
LC3s↑, Eugenol also induced autophagy by upregulating the expression levels of microtubule-associated protein 1 light chain 3 (LC3)
TumCI↓, Eugenol treatment shows an anti-metastatic effect by reducing the invasion and migration of MDA-MB-231 breast cancer cells mostly by reducing the expression of MMP-2 and MMP-9 [35].
TumMeta↓,
MMP2↓,
MMP9↓,
E2Fs↓, eugenol suppresses E2F1/survivin and triggers apoptosis in breast cancer cells
survivin↓,
BAX↑, eugenol can enhance Bax, thereby increasing cytochrome C while activating the caspase pathway required for apoptosis
Cyt‑c↑,

1293-

Ins,

Inositol Hexaphosphate Inhibits Growth and Induces G1 Arrest and Apoptotic Death of Androgen-Dependent Human Prostate Carcinoma LNCaP Cells

vitro+vivo,

Pca,

LNCaP

TumCG↓,
TumCCA↑, increase in G1 cell population
P21↑,
CDK4↓,
cycD1/CCND1↓,
RB1↑,
E2Fs↓,

222-

MFrot,

MF,

LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway

in-vitro,

Lung,

A549

 0.4T, 7.5 Hz

 inhibits iron metabolism

TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

5253-

NCL,

Niclosamide: Beyond an antihelminthic drug

Review,

Var,

TumCP↓, Niclosamide was found to inhibit adrenocortical carcinoma cellular proliferation, which was associated with apoptosis, reduction of epithelial-to-mesenchymal transition and β-catenin levels.
Apoptosis↑,
EMT↓,
β-catenin/ZEB1↓,
TumCG↓, Oral administration of niclosamide led to tumor growth inhibition with no observed toxicity.
toxicity↓,
Wnt↓, Lu et al. reported that niclosamide inhibits Wnt/β-catenin signaling by promoting Wnt co-receptor LRP6 degradation in breast cancer cells [11].
LRP6↓,
eff↑, niclosamide acts synergistically with a monoclonal antibody that specifically activates TRAIL death receptor 5 to inhibit tumor growth of basal-like breast cancers [12].
DR5↑,
mTORC1↓,
pH↓, Niclosamide lowered the cytoplasmic pH and may indirectly lead to inhibition of mTORC1 signaling [13]
CSCs↓, Niclosamide also was found to prevent the conversion of non-breast cancer stem cells into cancer stem cells
IL6↓, This mechanism is associated with inhibition of the IL6-JAK1-STAT3 signal transduction pathway
JAK1↓,
STAT3↓, Ren et al. identified niclosamide as a potent STAT3 inhibitor able to suppress STAT3 transcriptional activity
ChemoSen↑, niclosamide alone or in combination with cisplatin represses the growth of xenografts of cisplatin-resistant triple-negative breast cancer cells.
TumCG↓, Niclosamide inhibited growth of colon cancer cells from human patients both in vitro and in vivo, regardless of mutations in APC [24].
tumCV↓, niclosamide selectively inhibited glioblastoma cell viability [29]. Detailed mechanism studies revealed that niclosamide suppressed the Wnt, Notch, mTOR, and NF-κB signaling pathways.
NOTCH↓,
NF-kB↓,
EGFR↓, Li et al. reported that inhibition of EGFR by erlotinib, an FDA-approved therapeutic agent, led to activation of STAT3 signaling in head and neck cancer cells
ROS↑, niclosamide inhibits TNF-α-induced NF-κB–dependent reporter activity and increased the levels of reactive oxygen species (ROS) in AML cells.
RadioS↑, niclosamide enhanced radiosensitivity of the non-small cell lung cancer cell line H1299.
cFos↓, inhibit osteosarcoma cell proliferation, migration, and survival. This inhibitory effect is associated with decreased expression of c-Fos, c-Jun. E2F1, and c-Myc.
cJun↓,
E2Fs↓,
cMyc↓,
Half-Life↓, Niclosamide exhibits a short half-life (6.0 ± 0.8 h). Niclosamide was rapidly absorbed with a Tmax of less than 30 min. The Cmax is 354 ± 152 ng/mL.
BioAv↝, AUC and bioavailability were 429 ± 100 and 10%, respectively. In order to make more effective use of niclosamide, additional work needs to be done to improve its solubility, absorption and systemic bioavailability.

5254-

NCL,

The magic bullet: Niclosamide

Review,

Var,

Wnt↓, In particular, niclosamide inhibits multiple oncogenic pathways such as Wnt/β-catenin, Ras, Stat3, Notch, E2F-Myc, NF-κB, and mTOR and activates tumor suppressor signaling pathways such as p53, PP2A, and AMPK.
β-catenin/ZEB1↓,
RAS↓,
STAT3↓,
NOTCH↓,
E2Fs↓,
mTOR↓,
eff↑, Moreover, niclosamide potentially improves immunotherapy by modulating pathways such as PD-1/PDL-1.
PD-1↓,
PD-L1↓, primarily through PD-L1 ligand downregulation in cancer cells.
BioAv↝, The original pharmacokinetics study showed that the maximal serum concentration can reach 0.25-6.0ug/ml (0.76-18.34 µM) following administration of a single 2g dose (11).
toxicity↓, a strong safety profile and tolerability in humans.
BioAv↑, A potential solution to the aforementioned challenge is niclosamide ethanolamine (NEN), a salt form of niclosamide that also functions as a mitochondrial uncoupler with a superior safety profile and enhanced bioavailability
ETC↑, NEN activates the ETC to boost NADH oxidation, thereby leading to an increased intracellular NAD+/NADH ratio and driving the TCA cycle forward.
NADH:NAD↓,
TCA↑,
Warburg↓, leading to a reversal of the Warburg effect and the induction of cellular differentiation
Diff↑,
AMPK↑, figure 3
P53↑,
PP2A↑,
HIF-1↓,
KRAS↓,
Myc↓,
RadioS↑, leading to a reversal of the Warburg effect and the induction of cellular differentiation
ChemoSen↑, Niclosamide has shown synergistic anti-tumor effects with a broad spectrum of chemotherapy drugs.
Dose↝, In this trial, either 500mg or 1000mg niclosamide was given three times daily to patients. However, the maximal plasma concentration ranged from 35.7–82 ng/mL (0.1µM-0.25 µM), a range that failed to be consistently above the minimum effective concent
Dose↑, In contrast, the ongoing clinical trial NCT02807805 is administering 1200 mg of reformulated orally bioavailable niclosamide orally (PO) three times daily to patients, resulting in 0.21µM-0.723 plasma niclosamide concentrations exceeding the therape

58-

QC,

doxoR,

Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin

in-vitro,

CRC,

HT-29

 75 uM

in-vitro,

NA,

CD133+

CSC

Bcl-2↓,
TumCCA↑, Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin
CD133↓,
CSCs↓,
ChemoSen↑, adding quercetin to Dox chemotherapy is an effective strategy for treatment of both CSCs and bulk tumor cells.
CycB/CCNB1↑, Quer induces G2/M phase accumulation due to enhanced level of the cyclin B and decreased level of the cyclin E, cyclin D, E2F1, and E2F2
cycE/CCNE↓,
cycD1/CCND1↓,
E2Fs↓,

40-

QC,

Quercetin arrests G2/M phase and induces caspase-dependent cell death in U937 cells

in-vitro,

lymphoma,

U937

cycD1/CCND1↓, dramatic changes in the level of cyclin B, cyclin D, and cyclin E
cycE/CCNE↓,
E2Fs↓,
CycB/CCNB1↑, The G2/M phase accumulation was accompanied by an increase in the level of the cyclin B.
Casp↑, These data clearly indicate that quercetin-induced apoptosis is associated with caspase activation
Apoptosis↑,
TumCCA↑, We report here that quercetin induces anti-proliferation and arrests G2/M phase in U937 cells.
TumCP↓,

100-

QC,

Inhibition of Prostate Cancer Cell Colony Formation by the Flavonoid Quercetin Correlates with Modulation of Specific Regulatory Genes

in-vitro,

Pca,

PC3

 0-50 uM

in-vitro,

Pca,

DU145

in-vitro,

Pca,

LNCaP

cycD1/CCND1↓, CCND1, CCND2, CCND3
cycE/CCNE↓, CCNE1, CCNE2
CDK2↓,
CDK4/6↓, CDK4, CDK8
E2Fs↓, E2F2, E2F3
PCNA↓,
cDC2↓,
PTEN↑,
MSH2↑,
P21↑,
EP300↑, p300
BRCA1↑,
NF2↑,
TSC1↑,
TGFβR1↑, TGFβR2
P53↑,
RB1↑, Rb
AKT1↓,
cMyc↓,
CDC7↓,
cycF↓, CCNF
CDC16↓,
CUL4B↑, CUL4B, a member of the cullin gene family that is also known to be involved in control of the cell cycle, was significantly up-regulated by quercetin.
CBP↑,
TSC2↑,
HER2/EBBR2↓, erb-2
BCR↓,
TumCCA↑, quercetin significantly inhibited the expression of specific oncogenes and genes controlling G1, S, G2, and M phases of the cell cycle.
chemoPv↑, Our results correlate with those of nutritional studies that support the roles of dietary bioflavonoids as cancer chemopreventive agents.

3323-

SIL,

Anticancer therapeutic potential of silibinin: current trends, scope and relevance

Review,

Var,

Inflam↓, Silibinin has been shown to have anti-inflammatory, anti-angiogenic, antioxidant, and anti-metastatic properties
angioG↓,
antiOx↑,
TumMeta↓,
TumCP↓, silibinin helps in preventing proliferation of the tumor cells, initiating the cell cycle arrest, and induce cancer cells to die
TumCCA↑,
TumCD↑,
α-SMA↓, figure
p‑Akt↓,
p‑STAT3↓,
COX2↓,
IL6↓,
MMP2↓,
HIF-1↓,
Snail↓,
Slug↓,
Zeb1↓,
NF-kB↓,
p‑EGFR↓,
JAK2↓,
PI3K↓,
PD-L1↓,
VEGF↓,
CDK4↓,
CDK2↓,
cycD1/CCND1↓,
E2Fs↓,

3427-

TQ,

Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets

ROS⇅, It appears that the cellular and/or physiological context(s) determines whether TQ acts as a pro-oxidant or an anti-ox- idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in different cancer cells have been observed with 5-fluorouracil in gastric cancer and colorectal cancer models

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GPx1↑, 1, GSTs↑, 1, lipid-P↓, 1, ROS↓, 1, SOD1↑, 1,

Immune & Inflammatory Signaling ⓘ

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

Drug Metabolism & Resistance ⓘ

BioAv↑, 3, BioAv↝, 1,

Clinical Biomarkers ⓘ

IL6↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, toxicity↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 17

Scientific Paper Hit Count for: E2Fs, E2F family of transcription factors

3 Eugenol
3 Quercetin
2 Niclosamide (Niclocide)
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Inositol
1 Magnetic Field Rotating
1 Magnetic Fields
1 doxorubicin
1 Silymarin (Milk Thistle) silibinin
1 Thymoquinone

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

E2Fs Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

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 ⓘ

Cellular Microenvironment ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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