TS Cancer Research Results

TS, thymidylate synthase: Click to Expand ⟱
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Thymidylate synthase (TS) is a key enzyme responsible for catalyzing the methylation of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), a crucial step in the synthesis of thymidine—one of the four nucleotides required for DNA replication and repair.
Due to its essential role in DNA synthesis, TS is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and other antifolates.
Many cancers exhibit elevated levels of TS expression compared to normal tissues.
High TS expression can contribute to rapid cell proliferation and tumor growth by ensuring a sufficient supply of thymidine for DNA synthesis.

Thymidylate synthase (TS) plays a central role in DNA synthesis and cell proliferation, making it a critical enzyme in cancer biology. Overexpression of TS is commonly observed in a range of tumor types and is associated with increased cellular proliferation, drug resistance, and generally poorer clinical outcomes. As both a therapeutic target and a prognostic marker, TS levels offer insight into tumor aggressiveness and potential responsiveness to chemotherapeutic agents.
Scientific Papers found: Click to Expand⟱
2263- dietMet,    Methionine Restriction and Cancer Biology
- Review, Var, NA
AntiCan↑, dependence of many tumor cells on an exogenous source of the sulfur amino acid, methionine, [9,10,11] makes dietary methionine restriction (MR) an exciting potential tool in the treatment of cancer.
TumCP↓, Proliferation and growth of several types of cancer cells are inhibited by MR,
TumCG↓,
selectivity↑, while normal cells are unaffected by limiting methionine as long as homocysteine is present
ChemoSen↓, MR has been shown to enhance efficacy of chemotherapy and radiation therapy in animal models
RadioS↑,
Insulin↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis
*GlucoseCon↑, increase in tissue-specific glucose uptake measured during a hyperinsulinemic-euglycemic clamp
*ROS↓, MR does not increase oxidative stress, in part because MR enhances antioxidant capacity and increases proton leak in the liver, likely decreasing ROS production
*antiOx↑,
*GSH↑, ability of MR to increase GSH levels in red blood cells. Surprisingly, when methionine was restricted by 80% in the diet of rats, the level of GSH in the blood actually increased due to adaptations in sulfur-amino acid metabolism
GSH↑, However, GSH concentrations were reduced in the liver
eff↑, Of note, methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media.
polyA↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis, or by reducing polyamine synthesis. MR-induced depletion of polyamines
TS↓, MR selectively reduces TS activity in prostate cancer cells by ~80% within 48 h, but does not affect TS activity in normal prostate epithelial cells
Raf↓, MR inhibits Raf and Akt oncogenic pathways, while increasing caspase-9 and the mitochondrial pro-apoptotic protein, Bak
Akt↓,
Casp9↑,
Bak↑,
P21↑, MR upregulating p21 and p27 (cell cycle inhibitors that halt cell cycle progression) in LNCaP cells
p27↑,
Insulin↓, MR-induced reduction in circulating insulin and IGF1, which have both been linked to tumor growth
IGF-1↓,

2264- dietMet,    Methionine restriction for cancer therapy: From preclinical studies to clinical trials
- Review, Var, NA
TumCP↓, methionine restriction (MR) reduces cancer cell proliferation via different mechanisms
*ROS?, MR lowers sulfur-containing metabolite levels, reduces oxidative stress, and enhances the immune response
ChemoSen↑, may sensitize tumors to chemo/radiotherapy
RadioS↑,
eff↑, therapeutic potential of MR lies in its ability to synergize with other therapies, enhancing overall antitumor efficacy.
ROS↑, increases ROS, weaking cancer cell defense (from graphical abstract). In colon cancer, MR increases oxidative stress, induces cell cycle arrest, and promotes the apoptosis of p53(Tumor Protein 53)-deleted cells
selectivity↑, methionine-depleted media significantly impaired the growth of malignant cells while leaving normal cell growth unchanged.
TS↓, MR also targets thymidylate synthase (TS), a key enzyme in nucleotide synthesis, enhancing the chemotherapeutic efficacy of 5-FU by lowering TS activity and expression
eff↑, duration of methionine deprivation can significantly affect the tumor cell response. Intermittent methionine deprivation appears particularly beneficial, enhancing tumor cell sensitivity to CD8+ T cell-mediated cytotoxicity

1329- EMD,    Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cells
- in-vitro, Tong, SCC4
TumCCA↑, S-phase arrest
eff↓, The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis
P53↑,
P21↑,
p27↑,
cycA1/CCNA1↓,
cycE/CCNE↓,
TS↓,
CDC25↓, Cdc25A
AIF↑, promoted the release of apoptosis-inducing factor (AIF)
proCasp9↓,
Cyt‑c↑,
MMP↓,
Bax:Bcl2↑,
Casp3↑,
Casp9↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC25↓, 1,   Insulin↓, 2,   MMP↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

polyA↓, 1,   TS↓, 3,  

Cell Death ⓘ

Akt↓, 1,   Bak↑, 1,   Bax:Bcl2↑, 1,   Casp3↑, 1,   Casp9↑, 2,   proCasp9↓, 1,   Cyt‑c↑, 1,   p27↑, 2,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   cycE/CCNE↓, 1,   P21↑, 2,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   ChemoSen↑, 1,   eff↓, 1,   eff↑, 3,   RadioS↑, 2,   selectivity↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   ROS?, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↑, 1,  
Total Targets: 5

Scientific Paper Hit Count for: TS, thymidylate synthase
2 diet Methionine-Restricted Diet
1 Emodin
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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