TKT Cancer Research Results

TKT, transketolase: Click to Expand ⟱
Source:
Type:
Transketolase is a key enzyme in the non-oxidative arm of the pentose phosphate pathway (PPP), and alterations in its expression or activity can affect cellular metabolism, redox balance, and biosynthetic processes that are critical for rapidly proliferating cancer cells.

– Role: TKT catalyzes the reversible transfer of two-carbon units between sugars in the non-oxidative PPP.
– Impact: By contributing to the generation of ribose-5-phosphate for nucleotide synthesis and influencing the production of NADPH, TKT activity supports both biosynthetic demands and antioxidative defense in tumor cells.
-Alterations in TKT expression can therefore impact the balance between ROS generation and detoxification, influencing cell survival and chemoresistance.
-Inhibition of TKT may thus impair the cell’s antioxidative defenses, leading to a buildup of ROS. Elevated ROS can contribute to oxidative stress, damage cellular components, and in some contexts, even promote cell death.

– Many studies have observed that TKT is upregulated in various malignancies, including lung, breast, colon, and liver cancers.
– Association with Aggressiveness: Elevated TKT expression is often correlated with higher proliferation rates, enhanced anabolic activity, and worse clinical outcomes in some cancer types.
Scientific Papers found: Click to Expand⟱
2177- itraC,    Itraconazole improves survival outcomes in patients with colon cancer by inducing autophagic cell death and inhibiting transketolase expression
- Study, Colon, NA - in-vitro, CRC, COLO205 - in-vitro, CRC, HCT116
OS↑, Itraconazole increases the 5-year survival rate in patients with late-stage colon cancer who receive chemotherapy
tumCV↓, itraconazole decreased the viability and cell colony formation, and induced cleaved caspase-3 expression and G1 cell cycle arrest of COLO 205 and HCT 116 cells.
Casp3↑,
TumCCA↑,
HH↓, Itraconazole can induce autophagic cell death by activating the hedgehog pathway to inhibit breast cancer cell proliferation (25).
TumAuto↑, expression levels of the autophagy-related proteins, LC3B and p62, significantly increased in COLO 205 and HCT 116 cells following treatment with itraconazole for 24 h
LC3B↑,
p62↑,
TKT↓, TKT expression was decreased following treatment with itraconazole in a time-dependent manner


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

TKT↓, 1,  

Cell Death ⓘ

Casp3↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   p62↑, 1,   TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HH↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TKT, transketolase
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#:1258  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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