Selenate / Twist Cancer Research Results

Selenate, Selenate: Click to Expand ⟱

Features:

Selenate shares similarity with sulfate and enters cells via sulfate transporters; however, it is less readily reduced and often considered less potent in rapid cytotoxicity effects.

Selenate tends to exhibit higher IC50 values (often in the 10–100 µM range), indicating reduced potency compared to selenite in directly inducing cancer cell death.

Less Direct ROS Generation than Selenite.
– Selenate’s toxicity is generally less acute because it is a more inert species until metabolically reduced.
– It may exert its anticancer effects once it is converted into reduced selenium species that eventually can contribute to ROS production.

Twist, Twist: Click to Expand ⟱

Source:

Type: transcription factor

Twist, the basic helix-loop-helix transcription factor, is involved in the process of epithelial to mesenchymal transitions (EMTs), which play an essential role in cancer metastasis. Overexpression of Twist or its promoter methylation is a common scenario in metastatic carcinomas. Twist is a key transcription factor for Epithelial-mesenchymal transition (EMT).
Twist-1 overexpression was shown, recently, to be a factor of poor prognosis in melanomas Many studies use “TWIST” and “TWIST1” interchangeably (with TWIST1 being the canonical factor in humans.

Twist plays key roles in embryonic development and has been implicated in cancer progression, particularly through promoting epithelial-mesenchymal transition (EMT), invasion, and metastasis. TWIST1 directly represses epithelial markers (e.g., E-cadherin) while upregulating mesenchymal markers (e.g., N-cadherin, vimentin).

Twist is most often upregulated in cancer cells compared to normal cells across multiple tumor types.
– High Twist expression is consistently associated with aggressive clinical features, including increased invasiveness, metastasis, and reduced overall survival.

Scientific Papers found: Click to Expand⟱

1135-

Selenate,

Selenate induces epithelial-mesenchymal transition in a colorectal carcinoma cell line by AKT activation

in-vitro,

CRC,

DLD1

880uM

EMT↑, Akt↑, Twist↑, Vim↑, E-cadherin↓,

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:

Cell Death ⓘ

Akt↑, 1,

Proliferation, Differentiation & Cell State ⓘ

EMT↑, 1,

Migration ⓘ

E-cadherin↓, 1, Twist↑, 1, Vim↑, 1,
Total Targets: 5

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: Twist, Twist

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