Database Query Results : , , GLS

GLS, glutaminase: Click to Expand ⟱
Source:
Type:
Glutaminase is an enzyme that plays a crucial role in the metabolism of glutamine, an amino acid that is often utilized by cancer cells for growth and proliferation. In many cancers, including glioblastoma, leukemia, and certain types of solid tumors, glutamine metabolism is upregulated, allowing cancer cells to meet their increased energy and biosynthetic demands.
Glutamine Addiction: Many cancer cells exhibit a phenomenon known as "glutamine addiction," where they rely heavily on glutamine for survival and growth. This is particularly evident in rapidly proliferating tumors.
Glutaminase catalyzes the conversion of glutamine to glutamate, which can then enter various metabolic pathways, including the tricarboxylic acid (TCA) cycle. This process is essential for providing energy and building blocks for nucleotides and amino acids.
Inhibitors of glutaminase are being investigated in preclinical and clinical studies as a means to starve cancer cells of glutamine and inhibit their growth.

GLS expression is often elevated in various cancers and is generally associated with poorer prognosis due to its role in supporting the metabolic needs of cancer cells.
Scientific Papers found: Click to Expand⟱
2618- Ba,    Baicalein induces apoptosis by inhibiting the glutamine-mTOR metabolic pathway in lung cancer
- in-vitro, Lung, H1299 - in-vivo, Lung, A549
TumCG↓, Baicalein inhibited lung cancer xenograft tumor growth in vivo and suppressed proliferation and promoted apoptosis in lung cancer cells in vitro.
TumCP↓,
Apoptosis↑,
GLUT1↓, baicalein interacted with glutamine transporters as well as glutaminase and inhibited their activation
GLS↓,
mTOR↓, mTOR, an apoptosis-related protein and downstream target of glutamine metabolism, was also inhibited by baicalein treatment
*toxicity∅, baicalein treatment did not result in damage to the mouse organs, including the liver, heart, spleen, lung, or kidney
cl‑Casp9↓, baicalein dose-dependently suppressed the protein levels of Bax, cleaved caspase 9, and cleaved caspase 3 in H1299 and A549 cells
cl‑Casp3↓,
GSH↓, Meanwhile, the levels of glutathione (GSH), S-formylglutathione, and pyroglutamic acid in baicalein-treated A549 cells were downregulated when compared to that in control group
GlutMet↓, These findings indicate that baicalein inhibits cellular glutamine uptake, which is consistent with the findings of metabolomics studies.

2706- BBR,    Berberine Inhibits Growth of Liver Cancer Cells by Suppressing Glutamine Uptake
- in-vitro, HCC, Hep3B - in-vitro, HCC, Bel-7402 - in-vivo, NA, NA
TumCP↓, Berberine inhibited the proliferation of Hep3B and BEL-7404 cell in vitro
glut↓, Berberine suppressed the glutamine uptake by inhibiting SLC1A5.
SLC12A5↓,
cMyc↓, Berberine suppresses SLC1A5 expression by inhibiting c-Myc
GLS↓, The expression of SLC1A5, GLS and PSPH decreased, and such decrease was enhanced with the increase in berberine dose

1640- CA,  MET,    Caffeic Acid Targets AMPK Signaling and Regulates Tricarboxylic Acid Cycle Anaplerosis while Metformin Downregulates HIF-1α-Induced Glycolytic Enzymes in Human Cervical Squamous Cell Carcinoma Lines
- in-vitro, Cerv, SiHa
GLS↓, downregulation of Glutaminase (GLS) and Malic Enzyme 1 (ME1)
NADPH↓, CA alone and co-treated with Met caused significant reduction of NADPH
ROS↑, increased ROS formation and enhanced cell death
TumCD↑,
AMPK↑, activation of AMPK
Hif1a↓, Met inhibited Hypoxia-inducible Factor 1 (HIF-1α). CA treatment at 100 μM for 24 h also inhibited HIF-1α
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓, PFKFB4
PKM2↓,
LDH↓,
cMyc↓, Met suppressed the expression of c-Myc, BAX and cyclin-D1 (CCND1) a
BAX↓,
cycD1/CCND1↓,
PDH↓, CA at a concentration of 100 µM caused inhibition of PDK activity
ROS↑, CA Regulates TCA Cycle Supply via Pyruvate Dehydrogenase Complex (PDH), Induces Mitochondrial ROS Generation and Evokes Apoptosis
Apoptosis↑,
eff↑, both drugs inhibited the expression of ACLY and FAS, but the greatest effect was detected after co-treatment
ACLY↓,
FASN↓,
Bcl-2↓,
Glycolysis↓, Met acts as a glycolytic inhibitor under normoxic and hypoxic conditions

975- Est,    Estrogen inhibits autophagy and promotes growth of endometrial cancer by promoting glutamine metabolism
- vitro+vivo, UEC, NA
GLS↑, in estrogen-sensitive UEC cell (UECC) (an ER inhibitor antagonist) could reverse these effects.
cMyc↑, three MYC subtypes (c-MYC, n-MYC and l-MYC) were increased after estrogen treatment
GlutMet↑,
tumCV↑,
TumAuto↓,


* 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 ⓘ

GSH↓, 1,   ROS↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   AMPK↑, 1,   cMyc↓, 2,   cMyc↑, 1,   FASN↓, 1,   GLS↓, 3,   GLS↑, 1,   glut↓, 1,   GlutMet↓, 1,   GlutMet↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDH↓, 1,   NADPH↓, 1,   PDH↓, 1,   PFK↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↓, 1,   Bcl-2↓, 1,   cl‑Casp3↓, 1,   cl‑Casp9↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,   GLUT3↓, 1,   SLC12A5↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

LDH↓, 1,  
Total Targets: 37

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 1

Scientific Paper Hit Count for: GLS, glutaminase
1 Baicalein
1 Berberine
1 Caffeic acid
1 Metformin
1 Estrogen
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#:127  State#:%  Dir#:%
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