Akt2 Cancer Research Results
Akt2, RAC-beta serine/threonine-protein kinase: Click to Expand ⟱
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Enzyme that in humans is encoded by the AKT2 gene.
AKT2 is highly expressed in many human cancers, including non-small cell lung cancer (NSCLC). miR-124 overexpression can negatively regulate AKT2. knockout of both AKT1 and AKT2 will attenuate metastasis and tumor cell growth.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
BC, |
MDA-MB-231 |
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other↑, CoQ10 and UBIAD1 increase membrane fluidity leading to increased cell stiffness in BC
*antiOx↑, CoQ10 (or ubiquinone) is a potent lipid-soluble antioxidant enriched not only in mitochondria but also in plasma membranes
Risk↓, Loss of the CoQ10-biosynthetic enzyme UBIAD1 is associated to a worse prognosis in BC patients.
other↑, Deletion of Ubiad1 gene accelerates BC development in mouse models.
TumMeta↓, UBIAD1 expression limits metastasis formation in aggressive BC lines
ECM/TCF↓, CoQ10 and UBIAD1 expression impairs ECM-mediated signaling and AKT2 pathway in BC cells
Akt2↓,
Ferroptosis↑, UBIAD1 and CoQ10 enhance BC sensitivity to ferroptosis inducers via FSP1
eff↑, While CoQ10 treatment alone does not affect MDA-MB-231 cell viability, the co-treatment with RSL3 significantly enhanced cell death
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.
TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.
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:
Redox & Oxidative Stress ⓘ
Ferroptosis↑, 1, NRF2↓, 1, ROS↑, 2, SOD↓, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
BOK↑, 1, MMP↓, 1, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AKT1↓, 1, cMyc↓, 1, PPARγ↓, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↑, 2, BAD↑, 1, BAX↑, 1, Bcl-2↓, 1, BID↑, 2, cl‑Casp12↑, 1, Casp3↑, 2, Casp9↑, 2, Cyt‑c↑, 1, DR5↑, 1, FADD↑, 1, Fas↑, 1, Ferroptosis↑, 1, hTERT/TERT↓, 2, MAPK↓, 2, Mcl-1↓, 1, NAIP↓, 1, survivin↓, 1, Telomerase↓, 1,
Transcription & Epigenetics ⓘ
miR-21↓, 1, other↑, 2,
Protein Folding & ER Stress ⓘ
eIF2α↑, 1, ER Stress↑, 1, PERK↑, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, LC3II↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, DNMT1↓, 1, P53↓, 1, P53↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 2, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, ERK↓, 1, PI3K↓, 2, STAT5↓, 1, Wnt/(β-catenin)↓, 1,
Migration ⓘ
Akt2↓, 4, AP-1↓, 1, Ca+2↑, 1, E-cadherin↑, 1, miR-155↓, 1, MMP9↓, 1, N-cadherin↓, 1, TumCP↓, 3, TumMeta↓, 1, Vim↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, ATF4↑, 1, ECM/TCF↓, 1, p‑EGFR↓, 1, Hif1a↓, 1,
Immune & Inflammatory Signaling ⓘ
JAK2↓, 1, NF-kB↓, 3, PSA↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Clinical Biomarkers ⓘ
p‑EGFR↓, 1, hTERT/TERT↓, 2, PSA↓, 1,
Functional Outcomes ⓘ
Risk↓, 1,
Total Targets: 76
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, GSH↑, 1, NRF2↑, 1, ROS↓, 1, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
LDHA↑, 1,
Cell Death ⓘ
JNK↓, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↓, 1,
Migration ⓘ
Ca+2↝, 1,
Immune & Inflammatory Signaling ⓘ
IL1↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, neuroP↑, 2,
Total Targets: 20
Scientific Paper Hit Count for: Akt2, RAC-beta serine/threonine-protein kinase
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#:6 State#:% Dir#:1
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