STK11/LKB1 Cancer Research Results

STK11/LKB1, serine/threonine kinase 11: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
Also known as serine/threonine kinase 11
STK11, also known as LKB1 (Liver Kinase B1), is a tumor suppressor gene that plays a crucial role in regulating cell metabolism, growth, and polarity.
Enzymatic activity is crucial for regulating various cellular processes, including metabolism, cell growth, and cell cycle progression. The gene's role as a tumor suppressor is linked to its ability to control these processes, and mutations in STK11 can lead to the development of various cancers. In many cancers, particularly those associated with mutations in the STK11 gene, there is often a loss of STK11 expression or function.
Scientific Papers found: Click to Expand⟱
7630- Ins,    Modulation of both Insulin Resistance and Cancer Growth by Inositol
- Review, Var, NA - Review, Diabetic, NA
*IRes↓, number of synthetic and natural insulin sensitizers, including inositol, have been recognized to exert both anti-diabetic as well as anti-cancer properties.
*AntiDiabetic↑,
*glucose↝, beneficial effect of inositol in fostering glucose homeostasis as well as in antagonizing cancer growth.
AntiCan↑,
PI3K↓, NOSITOL INHIBITS THE PI3K/AKT PATHWAY IN CANCER CELLS
Akt↓,
Glycolysis↓, On the contrary, in cancer cells, IPGs and myo-Ins inhibits Akt reducing both glycolysis and glucose entry in the cell, while re-establishing the oxidative degradation of carbohydrates along the TCA.
STK11/LKB1↑, As inositol enhances specifically the LKB1 activity, it is worth noting that the AMPK-related anticancer activities are tightly dependent of that pathway
*FASN↓, Inositol inhibits fatty acids biosynthesis and reduces plasma LDL-cholesterol and non-esterified fatty acids (NEFA) levels [74-76].
*LDL↓,
*FFA/NEFA↓,
*ROS↓, Myo-Ins counteracts oxidative damage in fish exposed to environmental oxidative stress
ROS↑, anti-oxidant effects seem to be contextdependent, given that in cancer cells inositol actually increases free radical production
IGF-1↓, Furthermore, myoIns may likely inhibit IGF-1 release downstream of the induced inhibition

7800- ISQ,    Isoquercitrin Attenuates Oxidative Liver Damage Through AMPK-YAP Signaling: An Integrative In Silico, In Vitro, and In Vivo Study
- vitro+vivo, Nor, HepG2
*antiOx↑, Isoquercitrin, a flavonoid glycoside found in various plants, has demonstrated antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
*AntiCan↑,
*ROS↓, HepG2 cells exposed to arachidonic acid (AA) and iron exhibited oxidative stress-induced apoptosis, which was significantly attenuated by isoquercitrin treatment
*MMP↑, Isoquercitrin decreased reactive oxygen species (ROS) generation and preserved mitochondrial function in a dose-dependent manner.
*STK11/LKB1↑, isoquercitrin activates the LKB1/AMPK pathway, increasing phosphorylation of AMPK and its downstream target ACC, thereby modulating energy metabolism and reducing oxidative stress.
*AMPK↑,
*p‑AMPK↑,
*ACC↑,
*ALAT↓, isoquercitrin protected mice against carbon tetrachloride-induced liver injury, reducing serum ALT and AST levels and improving histopathological features.
*AST↓,
*hepatoP↑, isoquercitrin exerts hepatoprotective effects by activating the LKB1/AMPK pathway and modulating metabolic enzymes, highlighting its potential as a therapeutic agent against oxidative liver damage.

8150- lamb,    Reactive oxygen species dependent phosphorylation of the liver kinase B1/AMP activated protein kinase/ acetyl-CoA carboxylase signaling is critically involved in apoptotic effect of lambertianic acid in hepatocellular carcinoma cells
- in-vitro, HCC, HepG2 - in-vitro, HCC, SK-HEP-1
lipidLev↓, Though lambertianic acid (LA) is reported to have hypolipidemic activity in liver
TumCCA↑, LA increased cytotoxicity, sub-G1 population and Annexin V/PI positive cells in two HCC cells
cl‑Casp3↑, LA cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP), activated phosphorylation of liver kinase B1 (LKB1)/AMP activated protein kinase (AMPK)/ acetyl-CoA carboxylase (ACC) pathway
cl‑PARP↑,
AMPK↑,
Akt↓, also suppressed antiapoptotic proteins such as phosphorylation of Akt/ mammalian target of rapamycin (mTOR) and the expression of B cell lymphoma-2 (Bcl-2)/ B-cell lymphoma-extra large (Bcl-xL) and cyclooxygenase-2 (COX-2) in two HCC cells.
mTOR↓,
Bcl-2↓,
Bcl-xL↓,
COX2/PTGS2↓,
ROS↑, LA generated reactive oxygen species (ROS) in HepG2 cells
eff↓, AMPK inhibitor compound C or ROS inhibitor N-acetyl-L-cysteine (NAC) blocked the apoptotic ability of LA to cleave PARP or increase sub G1 population in HepG2 cells.
p‑STK11/LKB1↑, Overall, these findings suggest that ROS dependent phosphorylation of LKB1/AMPK/ACC signaling is critically involved in LA induced apoptosis in HCCs.
p‑ACC↑,
*Obesity↓, labmertianic acid (LA) is known to have anti-obesity [40], stress-protective [41], anti-allergic [42] and neurotropic
*Stress↓,
*antiAll↑,
tumCV↓, LA significantly suppressed the viability of HepG2, SK-Hep1 and Hep3B cells in a concentration dependent fashion, but not Chang normal hepatocyte cells.
selectivity↑,
TumCP↓, LA significantly inhibited proliferation of two HCC cells in a concentration and time dependent manner

8156- lamb,    A review on chemistry, source and therapeutic potential of lambertianic acid
- Review, Var, NA
*Obesity↓, potential health benefits in attenuating obesity, allergies and different cancers including breast, liver, lung and prostate cancer.
*AntiCan↑,
*AMPK↑, rats with high fat diet (HFD)-induced obesity by activating adenosine monophosphate activated protein kinase (AMPK)
*β-HEX↓, it was also observed that LA can suppress the release of β-hexosaminidase in a concentration-independent manner in BMMC
NA↑, anti-allergic activity
TumCCA↑, LA-treated MDA-MB-231 cells revealed that LA induces G2/ M phase arrest
AMPK↑, , LA activates AMPK and acetyl-CoA carboxylase (ACC) through phosphorylation and can suppress protein kinase B (AKT) phosphorylation,
ACC↑,
p‑Akt↓,
FOXM1↓, LA actively attenuates the expression of forkhead box protein M1 (FOXM1) and its regulated gene products, including proliferative proteins (Cyclin B1) and anti-apoptotic proteins (X-linked inhibitor of apoptosis protein [XIAP] and B-cell lymphoma 2 [
CycB/CCNB1↓,
XIAP↓,
Bcl-2↓,
p‑STAT3↓, LA suppresses the phosphorylation of STAT3 and NF-κB, the expression of p300 and RelA/ p65 acetylation,
p‑NF-kB↓,
Bcl-xL↓, LA blocks the expression of NF-κB regulated genes, including anti-apoptotic proteins (Bcl-2, Bcl-xL, XIAP and survivin), angiogenic protein vascular endothelial growth factor (VEGF), inflammatory protein COX-2, oncogenic genes cellular myelocytomato
survivin↓,
VEGF↓,
COX2/PTGS2↓,
cMyc↓,
IL6↓, and inflammatory mediators IL-6 and tumour necrosis factor-alpha (TNF-α) in the MCF-7 cells
TNF-α↓,
ROS↑, LA exhibits anticancer effects on hepatocellular carcinoma cells (HCC) through induction of apoptotic pathway by ROS-dependent activation of liver kinase B1 (LKB1)/AMPK/ ACC signalling cascades
STK11/LKB1↑,
cl‑Casp3↑, it induces the cleavage of caspase-3 and PARP along with the suppression of antiapoptotic proteins, Bcl-2 and Bcl-xl.
cl‑PARP↑,
eff↑, LA (20 μM) together with TRAIL (20 ng/ml) shows significant cytocidal effects in TRAIL resistant nonsmall cell lung cancer cell
AR↓, LA exerts anticancer effects by suppressing AR pathway in AR-sensitive prostate cancer cells LNCaP.
TumCP↓, 24 h LA treatment downregulates cell proliferation by reducing several protein levels, including p-53, p-p53, p21, p27, cyclin D1 and cell division kinase 4 (CDK4).
p‑P53↓,
P21↓,
p27/CDKN1B↓,
cycD1/CCND1↓,
CDK4↓,
PSA↓, LA exhibits anticancer properties by inhibiting AR expression and PSA in cellular and secretory levels
STAT3↓, LA induces apoptosis via miRNA-134 mediated inhibition of STAT3 and RelA/p65 acetylation
ac‑p65↓,
*antiAll↑, In conclusion, LA could be utilized in treating allergies, obesity and different cancers.


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:


NA, unassigned(tgid=0) ⓘ

NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↑, 1,   p‑ACC↑, 1,   AMPK↑, 2,   cMyc↓, 1,   Glycolysis↓, 1,   lipidLev↓, 1,   STK11/LKB1↑, 2,   p‑STK11/LKB1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Bcl-2↓, 2,   Bcl-xL↓, 2,   cl‑Casp3↑, 2,   p27/CDKN1B↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p‑P53↓, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↓, 1,   TumCCA↑, 2,  

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

FOXM1↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   IL6↓, 1,   p‑NF-kB↓, 1,   ac‑p65↓, 1,   PSA↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   FOXM1↓, 1,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiAll↑, 2,   FFA/NEFA↓, 1,   IRes↓, 1,   Stress↓, 1,   β-HEX↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↑, 1,   ALAT↓, 1,   AMPK↑, 2,   p‑AMPK↑, 1,   FASN↓, 1,   glucose↝, 1,   LDL↓, 1,   STK11/LKB1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 1,   hepatoP↑, 1,   Obesity↓, 2,  
Total Targets: 23

Scientific Paper Hit Count for: STK11/LKB1, serine/threonine kinase 11
2 lambertianic acid
1 Inositol
1 isoquercitrin
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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