WEE1 Cancer Research Results

WEE1, WEE1 G2 Checkpoint Kinase: Click to Expand ⟱
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WEE1 - WEE1 G2 Checkpoint Kinase

Abbreviation: WEE1

Type: Protein kinase / cell-cycle checkpoint kinase / DNA-damage response regulator

Function: WEE1 inhibits cyclin-dependent kinases, particularly CDK1 and CDK2, through inhibitory phosphorylation. This restrains S-phase progression and G2/M transition, prevents premature mitotic entry, stabilizes replication forks, and allows time for DNA-damage repair.

Cancer: ↑ WEE1 is frequently overexpressed or functionally relied upon in cancer cells, particularly tumors with defective TP53-dependent G1 checkpoint control. Increased WEE1 activity helps cancer cells tolerate replication stress and DNA damage by delaying cell-cycle progression and permitting repair.

Favorable Direction in Cancer: ↓ WEE1 activity is generally favorable in WEE1-dependent cancers because checkpoint inhibition can increase replication stress, prevent adequate DNA repair, force premature mitotic entry, and promote mitotic catastrophe and cancer-cell death.

Interpretation Note: WEE1 also has normal genome-protective functions in non-cancerous cells. Its cancer-promoting role is therefore best understood as tumor cells exploiting an otherwise protective checkpoint mechanism.
Scientific Papers found: Click to Expand⟱
8237- LCA,    Role of Licochalcone A in Potential Pharmacological Therapy: A Review
- Review, Var, NA
*other↝, Licorice always functions as an adjuvant drug in traditional Chinese medicine to reduce the toxicity of other medicinal herbs or enhance their pharmacological effects.
*Inflam↓, LA demonstrates various pharmacological properties, including anti-inflammation, antibacterial, antioxidant, anti-parasitic, bone protection, neuroprotection, skin protection, and blood glucose and lipid regulation.
*Bacteria↓,
*antiOx↑,
*AntiP↑,
*neuroP↑,
*glucose↝,
*lipid-P↓,
PKCδ↓, Downregulation of PKCε, p70S6K, and Akt is also described
P70S6K↓,
Akt↓,
ER Stress↑, LA induced ER stress in HepG2 cells to induce apoptosis
Apoptosis↑,
Ca+2↑, enhancing cytosolic Ca2+ release from the ER
PI3K↓, apoptosis of MCF-7 by inhibiting PI3K-Akt-mTOR signaling, thereby increasing caspase-3 activity, decreasing expression of B-cell lymphoma-2, and triggering the release of cytochrome from mitochondria into the cytoplasm
mTOR↓,
Casp3↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑, upregulation of Bax expression and PARP cleavage, downregulation of Bcl-2 and Cyclin D1, and accumulation of reactive oxygen species (ROS)
cl‑PARP↑,
cycD1/CCND1↑,
ROS↑,
CHOP/DDIT3↑, CHOP expression was elevated in parallel
ERK↑, LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner.
p38↑,
JNK↓, LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy
IAP1↓,
XIAP↓,
survivin↓,
cFLIP↓,
RIP1↓,
EGFR↓, promoted the degradation of EGFR, Met, Her2
MET↓,
HER2/EBBR2↓,
p‑4E-BP1↓, LA may inhibit the phosphorylation of 4EBP1 (Ser 65) and activate the PERK-eIF2α pathway to inhibit PD-L1 translation
PERK↑,
eIF2α↑,
PD-L1↓,
HK2↓, Hexokinase 2Â (HK2) expression was downregulated at a lower dose, attenuating glycolysis elevation and inducing apoptosis in MKN-45 and SGC7901 cells
Glycolysis↓,
Sp1/3/4↓, LA induced apoptosis via downregulating the expression of specificity protein 1 (Sp1), upregulating Bax, Bid, Bcl-xl, caspase-3, and PARP cleavage with doses of 10–40 μM
FasL↑, LA induced apoptosis in KB cells, relying on activation of caspase-dependent factor associated suicide ligand (FasL) mediated death receptor pathway.
MMP↓, reducing mitochondrial membrane potential and inhibiting ATP production in vitro
ATP↓,
TumAuto↑, The literature also showed that LA induced apoptosis and autophagy in SiHa
WEE1↑, LA blocked the cell cycle in HepG2 cells by increasing the expression of Weel, P21, Cyclin D1, and JNK1 and decreasing the expression of Survivin, Cyclin B1, and CDK1 using doses of 30–70 μM
P21↑,
CDK1↓,
TumCCA↑,
TumCMig↓, LA exhibited the ability to inhibit migration and invasion of A549 and H460 cells at relatively lower doses (2–20 μM)
TumCI↓,
ABCG2↓, downregulating the expression of breast cancer resistance protein (BCRP)
HSP90↓, LA also reduced Hsp90 activity in gefitinib-resistant NSCLC cells (H1975) via binding to the N-terminal ATP binding site of Hsp90 to reduce drug resistance
T-Cell↑, LA (40 mg/kg) to C3H/HeN mice bearing UM-UC-3 cells enhanced the activity of cytotoxic T lymphocytes and counts of CD4+ CD25+ Foxp3+ T regulatory T cells. Thus, LA might treat bladder cancer by modulating the tumor immune microenvironment
CD4+↑,
CD25+↑,
FOXP3↑,
Imm↝,
*Inflam↓, LA demonstrates anti-inflammatory activity via interaction with MAPK, NF-κB, NLRP3, and Nrf2 signaling in the acute lung, kidney, and liver injury (acute inflammation) and arthritis and asthma
*NF-kB↓,
*NRF2↑,
*AntiArt↑,

8244- LCA,    Licochalcone A from licorice root, an inhibitor of human hepatoma cell growth via induction of cell apoptosis and cell cycle arrest
- in-vitro, Liver, HepG2
TumCP↓, LCA inhibited the proliferation of HepG2 cells with IC50 (65.96 μM) for 24 h and IC50 (44.13 μM) for 48 h and caused significant morphological changes and also led to intracellular ROS generation.
ROS↑,
TumCCA↑, LCA affected HepG2 cell growth by terminating cell cycle development at G2/M transition and further induced the apoptosis process.
Apoptosis↑,
survivin↓, The mRNA expression of genes involved in cell cycles such as Survivin, Cyclin B1, and CDK1 were reduced
CycB/CCNB1↓,
CDK1↓,
WEE1↑, while, Weel, P21, Cyclin D1, and JNK1 showed increased mRNA expression.
P21↑,
cycD1/CCND1↑,
JNK↑,
TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, The anti-cancer action involved increased mRNA expression of DR3, DR5, caspases-3, caspases-8, caspases-10, Fas, Bad, Bax, Bcl-2, Bak, and PUMA
DR5↑,
Casp3↑,
Casp8↑,
Casp10↑,
Fas↑,
BAD↑,
BAX↑,
PUMA↑,
PKCδ↓, besides, decreased level of PKCε, p70S6K, and Akt.
P70S6K↓,
Akt↓,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, 1,   WEE1↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,   HK2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAD↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   Casp10↑, 1,   Casp3↑, 2,   Casp8↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 1,   FasL↑, 1,   IAP1↓, 1,   JNK↓, 1,   JNK↑, 1,   p38↑, 1,   PUMA↑, 1,   RIP1↓, 1,   survivin↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   HSP90↓, 1,   PERK↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↑, 2,   P21↑, 2,   TumCCA↑, 2,  

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

p‑4E-BP1↓, 1,   ERK↑, 1,   mTOR↓, 1,   P70S6K↓, 2,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   MET↓, 1,   PKCδ↓, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 1,   FOXP3↑, 1,   Imm↝, 1,   PD-L1↓, 1,   T-Cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,   PD-L1↓, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiP↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   lipid-P↓, 1,   NRF2↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↝, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,   NF-kB↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: WEE1, WEE1 G2 Checkpoint 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

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