TSC1 Cancer Research Results

TSC1, tuberous sclerosis 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
The TSC1 gene, located on chromosome 9, encodes a protein called hamartin, which plays a crucial role in regulating cell growth and proliferation. Mutations in the TSC1 gene are associated with tuberous sclerosis complex (TSC), a genetic disorder characterized by the development of benign tumors in various organs.

TSC1 (hamartin) and TSC2 (tuberin) form a complex that plays a critical role in regulating the mTOR (mechanistic target of rapamycin) pathway.
• The TSC1/TSC2 complex acts as a negative regulator of mTOR signaling; when active, it helps suppress cell growth and proliferation.

TSC1 and TSC2 serve as tumor suppressors.
TSC1 and TSC2 are not overexpressed in cancer; they are typically involved in loss-of-function scenarios that lead to tumorigenesis.
Scientific Papers found: Click to Expand⟱
1608- EA,    Ellagic Acid from Hull Blackberries: Extraction, Purification, and Potential Anticancer Activity
- in-vitro, Cerv, HeLa - in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, HUVECs
eff↑, Hull blackberry fruits into five growth periods according to color and determined the EA content in the fruits in each period. The EA content in the green fruit stage was the highest at 5.67 mg/g FW
Dose∅, EA inhibited HeLa cells with an IC50 of 35 μg/mL
*BioAv↑, EA is not sensitive to high temperatures and is not highly soluble in many solvents.
selectivity↑, selectivity index varied from 7.4 for Hela to about 1 for A549
TumCP↓, EA reduced the proliferation of human cervical cancer HeLa, SiHa, and C33A cells in a dose- and time-dependent manner, and the inhibitory effect was significantly more pronounced in HeLa cells than in SiHa and C33A cells
Casp↑, EA reduced the proliferation of human cervical cancer HeLa, SiHa, and C33A cells in a dose- and time-dependent manner, and the inhibitory effect was significantly more pronounced in HeLa cells than in SiHa and C33A cells
PTEN↑,
TSC1↑,
mTOR⇅,
Akt↓, AKT, PDK1 expression were down-regulated
PDK1↓,
E6↓, mRNA levels of E6/E7 were determined to decrease gradually with the increase in EA incubation time and concentration
E7↓,
DNAdam↑, When DNA damage is introduced into cells from exogenous or endogenous sources there is an increase in the amount of intracellular reactive oxygen species (ROS)
ROS↑,
*BioAv↓, EA cannot be exploited for in vivo therapeutic applications in the current situation because of its poor water solubility and accordingly low bioavailability.
*BioEnh↑, As Lei [52] reported that EA in pomegranate leaf is rapidly absorbed and distributed as well as eliminated in rats
*Half-Life∅, blood concentration peaked at 0.5 h with Cmax = 7.29 μg/mL, and the drug concentration decreased to half of the original after 57 min of administration

100- QC,    Inhibition of Prostate Cancer Cell Colony Formation by the Flavonoid Quercetin Correlates with Modulation of Specific Regulatory Genes
- in-vitro, Pca, PC3 - 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.


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:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

BCR↓, 1,   CDC16↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   cMyc↓, 1,   PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Casp↑, 1,   CBP↑, 1,  

Kinase & Signal Transduction ⓘ

CDC7↓, 1,   HER2/EBBR2↓, 1,   TSC2↑, 1,  

DNA Damage & Repair ⓘ

BRCA1↑, 1,   CUL4B↑, 1,   DNAdam↑, 1,   P53↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   cycF↓, 1,   E2Fs↓, 1,   P21↑, 1,   RB1↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

cDC2↓, 1,   EP300↑, 1,   mTOR⇅, 1,   NF2↑, 1,   PTEN↑, 2,  

Migration ⓘ

CDK4/6↓, 1,   MSH2↑, 1,   TSC1↑, 2,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose∅, 1,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BRCA1↑, 1,   E6↓, 1,   E7↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   TGFβR1↑, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioEnh↑, 1,   Half-Life∅, 1,  
Total Targets: 4

Scientific Paper Hit Count for: TSC1, tuberous sclerosis 1
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#:318  State#:%  Dir#:2
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