AKT1 Cancer Research Results

AKT1, v-akt murine thymoma viral oncogene homolog 1: Click to Expand ⟱

Source: CGL-Driver Genes

Type: Oncogene

RAC‑α serine/threonine‑protein kinase (commonly referred to as AKT1)
It is known as the “survival kinase”. Akt mediates cell survival proliferation mainly by inhibiting the Bcl2 and MDM2 pathways, which otherwise promotes apoptosis.
Mechanisms of Akt1 in Cancer
Cell Survival: Akt1 promotes cell survival by inhibiting apoptotic pathways, allowing cancer cells to evade programmed cell death.
Cell Proliferation: It enhances cell cycle progression and proliferation through various signaling pathways.
Metabolism: Akt1 regulates glucose metabolism and lipid synthesis, supporting the metabolic demands of rapidly dividing cancer cells.
Angiogenesis: It promotes the formation of new blood vessels, facilitating tumor growth and metastasis.

Akt1 is frequently activated, with its expression levels often correlating with prognosis across various cancer types.

Scientific Papers found: Click to Expand⟱

5363-

AV,

Exploring the mechanism of aloe-emodin in the treatment of liver cancer through network pharmacology and cell experiments

Study,

HCC,

AKT1↓, The involvement of AKT1 and EGFR, as well as the key target of the PI3K-AKT signaling pathway, indicated the importance of this signaling pathway in the treatment of HCC using AE.
EGFR↓,
PI3K↓, The downregulation of EGFR, PI3KR1, AKT1, and BCL2 in mRNA expression and PI3KR1, AKT,p-AKT in protein expression confirmed our hypothesis.
Bcl-2↓,
TumCG↓, AE inhibited hepatic cancer cell growth in vitro
Apoptosis↑, AE induced apoptosis of HCC cells

1261-

CAP,

Capsaicin inhibits glycolysis in esophageal squamous cell carcinoma by regulating hexokinase‑2 expression

in-vitro,

ESCC,

KYSE150

GlucoseCon↓,
lactateProd↓,
HK2↓,
Glycolysis↓,
PTEN↑,
AKT1↓, RAC‑α serine threonine‑protein kinase signaling pathway was downregulated

6034-

CGA,

Effect and mechanism of chlorogenic acid on cognitive dysfunction in mice by lipopolysaccharide-induced neuroinflammation

in-vivo,

AD,

mice

*cognitive↑, Chlorogenic acid can inhibit microglial polarization toward the M1 phenotype and improve neuroinflammation-induced cognitive dysfunction in mice by modulating these key targets in the TNF signaling pathway.
*TNF-α↓,
*antiOx↑, strong antioxidant and anti-inflammatory effects of CGA, many scholars have found that it has a good neuroprotective effect
*Inflam↓,
*neuroP↑,
*BBB↑, CGA is able to cross the blood-brain barrier (BBB) and can treat certain neurological disorders (
*eff↑, Several clinical and preclinical studies have shown that coffee extract (CGA, the main component) exhibits good therapeutic effects in Alzheimer’s disease and Parkinson’s disease
*memory↑, CGA improved memory loss and hippocampal cell death after transient total cerebral ischemia
*AKT1↓, Chlorogenic acid inhibited LPS-induced activation of Akt1, TNF, MMP9, PTGS2, MAPK1, MAPK14, and RELA targets in the TNF signaling pathway
*MMP9↓,
*MAPK↓,

6069-

CHL,

PDT,

Anti-Cancer Effect of Chlorophyllin-Assisted Photodynamic Therapy to Induce Apoptosis through Oxidative Stress on Human Cervical Cancer

in-vitro,

Cerv,

HeLa

eff↑, chlorophyllin-assisted photodynamic therapy significantly induced cytotoxicity
ROS↑, In addition, reactive oxygen species generation and Annexin V expression level were detected on the photodynamic reaction-treated HeLa cells under the optimized conditions to evaluate apoptosis using a fluorescence microscope.
Casp8↓, the photodynamic therapy group showed the increased protein expression level of the cleaved caspase 8, caspase 9, Bax, and cytochrome C, and the suppressed protein expression level of Bcl-2, pro-caspase 8, and pro-caspase 9.
Casp9↑,
BAX↑,
Cyt‑c↑,
Bcl-2↓,
AKT1↓, the proposed photodynamic therapy downregulated the phosphorylation of AKT1 in the HeLa cells.

2787-

CHr,

Network pharmacology unveils the intricate molecular landscape of Chrysin in breast cancer therapeutics

Analysis,

Var,

MCF7

22.55 µM

TumCP↓, implicated in cell proliferation, angiogenesis, invasion, and metastasis
angioG↓,
TumCI↓,
TumMeta↓,
TP53↑, Chrysin exhibited strong binding interactions with several key hub proteins, notably TP53, AKT1, and CASP3, suggesting its capacity to inhibit tumorigenesis in breast cancer
Akt↓,
Casp3↑,
tumCV↓, dose-dependent reduction in cell viability was observed, with an IC50 value of 67.43 and 22.55 µM for 24 and 48 h
TNF-α↓, chrysin binds strongly to TNF-α, potentially inhibiting its function.
BioAv↑, Improved bioavailability of chrysin via its interaction with HSA could enhance its therapeutic efficacy, a factor that could be further explored in future pharmacokinetic studies
BioAv↑, Albumin’s ability to bind and transport Chrysin could influence the bioavailability of the flavonoid, potentially enhancing its therapeutic effects.
AKT1↓, chrysin effectively inhibits AKT1,

6352-

DRE,

Investigation of the Anti-Lung Cancer Mechanisms of Taraxacum officinale Based on Network Pharmacology and Multidimensional Experimental Validation

in-vitro,

Lung,

A549

in-vitro,

Nor,

L929

other↝, Our analyses identified 58 active compounds in dandelion linked to 614 potential targets, of which 228 targets were associated with LC.
other↝, six key targets—TP53, CASP3, EGFR, AKT1, ESR1, and NQO1—were selected for molecular docking with four major active compounds: quercetin, apigenin, kaempferol, and luteolin.
tumCV↑, viability of A549 cells progressively decreased with increasing taraxasterol concentration and treatment duration, with the most significant inhibitory effect observed at 25 μmol/L
selectivity?, At the same concentration, taraxasterol did not exhibit significant cytotoxicity toward normal L929 cells, with cell viability remaining at or above 80%
EGFR↓, six hub genes—TP53, CASP3, EGFR, AKT1, ESR1, and NQO1—were identified as potential key targets underlying the anti-lung cancer effects of dandelion.
AKT1↓,
NQO1↓,

6846-

EVO,

Evodiamine Inhibits Colorectal Cancer Growth via RTKs Mediated PI3K/AKT/p53 Signaling Pathway

in-vitro,

CRC,

HT29

in-vitro,

CRC,

HCT116

TumCP↓, The results demonstrated that EVO exerts inhibitory effects on CRC cell proliferation, invasion, and colony formation.
TumCI↓,
TumCCA↑, The cell cycle assay revealed that EVO induces G1/S phase arrest.
PI3K↓, possible mechanism of action is inhibiting the expression of the RTK protein family, activating the PI3K/AKT/p53 apoptotic signaling pathway, thereby inhibiting Bcl-2 expression and increasing Bax expression, promoting apoptosis of CRC cells.
AKT1↓, significant downregulation in the expression levels of AKT1, PI3K, EGFR, PDGFRα, and PDGFRβ, while the expression level of p53 exhibited a notable upregulation.
P53↑,
Bcl-2↓,
BAX↑,
Apoptosis↑,
p‑Casp9↑, phosphorylated caspase-9 expression increased significantly,
E-cadherin↑, fter EVO treatment of cells, E-cadherin expression increased, N-cadherin expression decreased, and MMP9 protein expression decreased.
N-cadherin↓,
MMP9↓,
CSCs↓, above results confirm once again that EVO has the ability to inhibit spatial metastasis of CRC cells.
EGFR↓, significant downregulation in the expression levels of AKT1, PI3K, EGFR, PDGFRα, and PDGFRβ, while the expression level of p53 exhibited a notable upregulation.
PDGFRA↓,
Dose↝, (BALB)/c nude mice. The EVO group was intraperitoneal injected with 10 mg/kg EVO, and the mock group was injected with an equal amount of saline.
TumCG↓, In summary, EVO can inhibit the growth of CRC in vivo.

7047-

GA,

Gallic acid-conjugated 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone induces apoptosis and downregulates PI3K/Akt signaling through VEGFR-2 targeting in non-small cell lung cancer (NSCLC)

in-vitro,

NSCLC,

A549

TumCP↓, In vitro 2D cytotoxicity assays demonstrated potent antiproliferative activity, with IC₅₀ values of 3.93 ± 0.47 μM in A549 and 4.88 ± 1.42 μM in non-small cell lung cancer (NSCLC) cells,
selectivity↑, while showing reduced cytotoxicity in normal fibroblasts (MRC-5; IC₅₀ = 10.48 ± 1.83 μM) compared with osimertinib.
AKT1↓, significant downregulation of PTGER4, AKT1, PDPK1, and PRKCA.
EP4/PTGER4↓,
PDK1↓,
VEGFR2/KDR/Flk1↓, strong binding affinity of compound 3 to the VEGFR-2 kinase domain, stabilizing critical active-site residues and supporting a structure-based mechanism of action.

7364-

HibSad,

Hibiscus sabdariffa calyx extract induces anti-proliferative and anti-migratory effects in ovarian cancer

in-vitro,

Ovarian,

OVCAR-3

*Inflam↓, known for its anti-inflammatory, antimicrobial, and antioxidant properties.
*AntiBio↑,
*antiOx↑,
TumCMig↓, 2.8 mg IC50 value, with atypical nuclear morphology and reduced cell migration.
AKT1↓, Rosella crude extract influences ECM1 glycoprotein, AKT1, and Cyclin D1 suppressing colony-forming ability.
cycD1/CCND1↓,

7456-

HNK,

Honokiol in the treatment of triple-negative breast cancer: a network pharmacology approach and experimental validation

vitro+vivo,

BC,

MDA-MB-231

 zebrafish xenograft model.

in-vitro,

BC,

MDA-MB-468

Apoptosis↑, Results indicated that HNK induces apoptosis in MDA-MB 231 and MDA-MB 468 cells and inhibits their migration and proliferation.
TumCMig↓,
TumCP↓,
HSP90↓, HNK targets against TNBC, including HSP90AA1, AKT1, EGFR, ERBB2, HSP90AB1, PGR, MDM2, HDAC1, NR3C1, and MAPK14.
AKT1↓,
EGFR↓,
HSP90↓,
MDM2↓,
HDAC1↓,

7642-

IP6,

Inositol Hexaphosphate Inhibits Proliferation and Induces Apoptosis of Colon Cancer Cells by Suppressing the AKT/mTOR Signaling Pathway

in-vitro,

CRC,

AntiCan↑, Inositol hexaphosphate (InsP6), a natural occurring phytochemical, has been shown to have both preventive and therapeutic effects against various cancers,
TumCP↓, The results revealed that IP6 inhibited proliferation and stimulated apoptosis of colon cancer cells.
Apoptosis↑,
P21↑, This effect was mediated by an increase in the expression of genes encoding p21, p27, caspase 3, caspase 9 as well a decrease in transcription of AKT1 and S6K1.
p27/CDKN1B↑,
Casp3↑,
Casp9↑,
AKT1↓,
S6K↓,
mTOR↓, InsP6 can reduce proliferation and induce apoptosis through inhibition of the AKT/mTOR pathway

2912-

LT,

Luteolin: a flavonoid with a multifaceted anticancer potential

Review,

Var,

ROS↑, induction of oxidative stress, cell cycle arrest, upregulation of apoptotic genes, and inhibition of cell proliferation and angiogenesis in cancer cells.
TumCCA↑,
TumCP↓,
angioG↓,
ER Stress↑, Luteolin induces mitochondrial dysfunction and activates the endoplasmic reticulum stress response in glioblastoma cells, which triggers the generation of intracellular reactive oxygen species (ROS)
mtDam↑,
PERK↑, activate the expression of stress-related proteins by mediating the phosphorylation of PERK, ATF4, eIF2α, and cleaved-caspase 12.
ATF4↑,
eIF2α↑,
cl‑Casp12↑,
EMT↓, Luteolin is known to reverse epithelial-to-mesenchymal transition (EMT), which is associated with the cancer cell progression and metastasis.
E-cadherin↑, upregulating the biomarker E-cadherin expression, followed by a significant downregulation of the N-cadherin and vimentin expression
N-cadherin↓,
Vim↓,
*neuroP↑, Furthermore, luteolin holds potential to improve the spinal damage and brain trauma caused by 1-methyl-4-phenylpyridinium due to its excellent neuroprotective properties.
NF-kB↓, downregulation and suppression of cellular pathways such as nuclear factor kappa B (NF-kB), phosphatidylinositol 3’-kinase (PI3K)/Akt, and X-linked inhibitor of apoptosis protein (XIAP)
PI3K↓,
Akt↑,
XIAP↓,
MMP↓, Furthermore, the membrane action potential of mitochondria depletes in the presence of luteolin, Ca2+ levels and Bax expression upregulate, the levels of caspase-3 and caspase-9 increase, while the downregulation of Bcl-2
Ca+2↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Cyt‑c↑, cause the cytosolic release of cytochrome c from mitochondria
IronCh↑, Luteolin serves as a good metal-chelating agent owing to the presence of dihydroxyl substituents on the aromatic ring framework
SOD↓, luteolin further triggered an early phase accumulation of ROS due to the suppression of the activity of cellular superoxide dismutase.
*ROS↓, Luteolin reportedly demonstrated an optimal 43.7% inhibition of the accumulation of ROS, 24.5% decrease in malondialdehyde levels, and 38.7% lowering of lactate dehydrogenase levels at a concentration of 30 µM
*LDHA↑,
*SOD↑, expression of superoxide dismutase ameliorated by 73.7%, while the activity of glutathione improved by 72.3% at the same concentration of luteolin
*GSH↑,
*BioAv↓, Poor bioavailability of luteolin limits its optimal therapeutic efficacy and bioactivity
Telomerase↓, MDA-MB-231 cells with luteolin led to dose dependent arrest of cell cycle in S phase by reducing the levels of telomerase and by inhibiting the phosphorylation of NF-kB inhibitor α along with its target gene c-Myc
cMyc↓,
hTERT/TERT↓, These events led to the suppression of the expression of human telomerase reverse transcriptase (hTERT) encoding for the catalytic subunit of telomerase
DR5↑, luteolin upregulated the expression of caspase cascades and death receptors, including DR5
Fas↑, expression of proapoptotic genes such as FAS, FADD, BAX, BAD, BOK, BID, TRADD upregulates, while the anti-apoptotic genes NAIP, BCL-2, and MCL-1 experience downregulation.
FADD↑,
BAD↑,
BOK↑,
BID↑,
NAIP↓,
Mcl-1↓,
CDK2↓, expression of cell cycle regulatory genes CDK2, CDKN2B, CCNE2, CDKN1A, and CDK4 decreased on incubation with luteolin
CDK4↓,
MAPK↓, expression of MAPK1, MAPK3, MAP3K5, MAPK14, PIK3C2A, PIK3C2B, AKT1, AKT2, and ELK1 downregulated
AKT1↓,
Akt2↓,
*Beclin-1↓, luteolin led to downregulation of the expression of hypoxia-inducible factor-1α and autophagy-associated proteins, Beclin 1, and LC3
Hif1a↓,
LC3II↑, LC3-II is upregulated following the luteolin treatment in p53 wild type HepG2 cells i
Beclin-1↑, Luteolin treatment reportedly increased the number of intracellular autophagosomes, as indicated by an increased expression of Beclin 1, and conversion of LC3B-I to LC3B-II in hepatocellular carcinoma SMMC-7721 cells.

2922-

LT,

Combination of transcriptomic and proteomic approaches helps unravel the mechanisms of luteolin in inducing liver cancer cell death via targeting AKT1 and SRC

in-vitro,

Liver,

HUH7

 12.68 µM

Half-Life↝, However, after oral administration, luteolin showed relatively rapid absorption and slow elimination in rats, with a tmax (time to reach peak plasma level) of approximately 1.02 h and a t1/2 (elimination half-life) of 4.94 h, indicating that luteolin
TumCCA↑, luteolin could promote cell cycle arrest and apoptosis in HuH-7 cells
AKT1↓, Dramatic downregulation of components downstream of the AKT1-ASK2-ATF2 pathway (CycD, BCL2, CycA, etc.), the AKT1-NF-κB pathway (BCL-XL and MIP2) and the AKT1-GSK3β-β-catenin pathway (c-Myc and CCND1)
ATF2↓,
NF-kB↓,
GSK‐3β↓,
cMyc↓,
GSTs↓, expression change of NQO-1, GSTs, and TRXR1 indicated the increase in ROS
TrxR1↓,
ROS↑,

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.

4912-

Sal,

Salinomycin induces cell death with autophagy through activation of endoplasmic reticulum stress in human cancer cells

in-vitro,

Lung,

A549

2.5 μM

in-vitro,

Lung,

H460

in-vitro,

Lung,

Calu-1

in-vitro,

Lung,

H157

CSCs↓, Salinomycin is perhaps the first promising compound that was discovered through high throughput screening in cancer stem cells.
TumAuto↑, salinomycin induced autophagy in human non-small cell lung cancer (NSCLC) cells
ER Stress↑, salinomycin stimulated endoplasmic reticulum stress and mediated autophagy via the ATF4-DDIT3/CHOP-TRIB3-AKT1-MTOR axis.
TumCD↑, salinomycin effectively decreased the survival of the indicated cells in a dose-dependent manner
ATF4↑, Salinomycin induces autophagy via ER stress-dependent upregulation of ATF4 and DDIT3
CHOP/DDIT3↑,
AKT1↓, salinomycin via AKT1-MTOR inhibition in human NSCLC cells.
mTOR↓,

3195-

SFN,

AKT1/HK2 Axis-mediated Glucose Metabolism: A Novel Therapeutic Target of Sulforaphane in Bladder Cancer

in-vitro,

Bladder,

UMUC3

ATP↓, SFN strongly downregulates ATP production by inhibiting glycolysis and mitochondrial oxidative phosphorylation (OXPHOS).
Glycolysis↓,
OXPHOS↓,
HK2↓, SFN weaken the glycolytic flux by suppressing multiple metabolic enzymes, including hexokinase 2 (HK2) and pyruvate dehydrogenase (PDH).
PDH↓,
AKT1↓, SFN decreases the level of AKT1 and p-AKT ser473 , especially in low-invasive UMUC3 cells.
p‑Akt↓,

2448-

SFN,

Sulforaphane and bladder cancer: a potential novel antitumor compound

Review,

Bladder,

Apoptosis↑, Recent studies have demonstrated that Sulforaphane not only induces apoptosis and cell cycle arrest in BC cells, but also inhibits the growth, invasion, and metastasis of BC cells
TumCG↓,
TumCI↓,
TumMeta↓,
glucoNG↓, Additionally, it can inhibit BC gluconeogenesis
ChemoSen↑, demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens.
TumCCA↑, SFN can block the cell cycle in G2/M phase, upregulate the expression of Caspase3/7 and PARP cleavage, and downregulate the expression of Survivin, EGFR and HER2/neu
Casp3↑,
Casp7↑,
cl‑PARP↑,
survivin↓,
EGFR↓,
HER2/EBBR2↓,
ATP↓, SFN inhibits the production of ATP by inhibiting glycolysis and mitochondrial oxidative phosphorylation in BC cells in a dose-dependent manner
Glycolysis↓,
mt-OXPHOS↓,
AKT1↓, dysregulation of glucose metabolism by inhibiting the AKT1-HK2 axis
HK2↓,
Hif1a↓, Sulforaphane inhibits glycolysis by down-regulating hypoxia-induced HIF-1α
ROS↑, SFN can upregulate ROS production and Nrf2 activity
NRF2↑,
EMT↓, inhibiting EMT process through Cox-2/MMP-2, 9/ ZEB1 and Snail and miR-200c/ZEB1 pathways
COX2/PTGS2↓,
MMP2↓,
MMP9↓,
Zeb1↓,
Snail↓,
HDAC↓, FN modulates the histone status in BC cells by regulating specific HDAC and HATs,
HATs↓,
MMP↓, SFN upregulates ROS production, induces mitochondrial oxidative damage, mitochondrial membrane potential depolarization, cytochrome c release
Cyt‑c↓,
Shh↓, SFN significantly lowers the expression of key components of the SHH pathway (Shh, Smo, and Gli1) and inhibits tumor sphere formation, thereby suppressing the stemness of cancer cells
Smo↓,
Gli1↓,
BioAv↝, SFN is unstable in aqueous solutions and at high temperatures, sensitive to oxygen, heat and alkaline conditions, with a decrease in quantity of 20% after cooking, 36% after frying, and 88% after boiling
BioAv↝, It has been reported that the ability of individuals to use gut myrosinase to convert glucoraphanin into SFN varies widely
Dose↝, Excitingly, it has been reported that daily oral administration of 200 μM SFN in melanoma patients can achieve plasma levels of 655 ng/mL with good tolerance

Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2, GSH↑, 1, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

AKT1↓, 1, LDHA↑, 1,

Cell Death(tgid=5) ⓘ

MAPK↓, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,

Migration(tgid=13) ⓘ

MMP9↓, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2, TNF-α↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, eff↑, 1,

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1, memory↑, 1, neuroP↑, 2,
Total Targets: 18

Scientific Paper Hit Count for: AKT1, v-akt murine thymoma viral oncogene homolog 1

2 Luteolin
2 Sulforaphane (mainly Broccoli)
1 Aloe anthraquinones
1 Capsaicin
1 Chlorogenic acid
1 Chlorophyllin
1 Photodynamic Therapy
1 Chrysin
1 Dandelion Root
1 Evodiamine
1 Gallic acid
1 Hibiscus sabdariffa
1 Honokiol
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Quercetin
1 salinomycin

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

AKT1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

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