KC7F2

KC7F2 inhibits HIF-1α protein synthesis but not its mRNA transcription. This compound inhibits HRE-driven transcription and decreases HIF-1α protein levels in LN229-HRE-AP cells. It shows a dose-response cytotoxicity with IC50 of approximately 15 to 25 μM in cancer cells MCF7, LNZ308, A549, U251MG, and LN229. In D54MG glioma cells, this chemical inhibits colony formation, especially under hypoxia. [1] In hypoxic microglial cultures, it downregulates the expression of TfR and DMT, and reduces the HIF-1α mediated iron accumulation. [2]

This compound significantly reduces the latent period in the pentylenetetrazole kindling rat model and increases the rate of spontaneous recurrent seizures during the chronic stage. [3]

• Saggio di attività trascrizionale HIF

  Le cellule vengono incubate a 37°C in un'atmosfera umidificata contenente 5% di CO₂ e 21% di O₂ (normossia) o 1% di O₂ (ipossia) in una workstation per ipossia. La linea cellulare reporter LN229-HRE-AP per l'attività trascrizionale di HIF viene creata trasfettando stabilmente le cellule LN229 con il plasmide pACN188, che contiene un gene per la fosfatasi alcalina guidato da sei HRE derivati dal gene VEGF.

• Linee cellulari

  Human dermal microvascular endothelial cells and mouse neurons; MCF7, LNZ308, A549, U251MG, and LN229 cell lines

• Concentrazioni

  72 h

• Tempo di incubazione

  20 μM

• Metodo

  Cells are seeded onto 96-well plates (4 × 10³/well) and cultured under normoxic (21% O₂) and hypoxic (1% O₂) conditions with different concentrations of KC7F2 for 72 h or treated for various times with 20 μM this compound. For proliferation analysis, cells are fixed with 50% trichloroacetic acid for 1 h at 4°C, followed by staining with 0.4% sulforhodamine B dissolved in 1% acetic acid for 30 min at room temperature. Plates are washed five times with 1% acetic acid to remove unbound dye. Bound dye is dissolved by adding 10 mM unbuffered Tris base. Cell proliferation is calculated by measuring OD values at 564 nm using a spectrophotometer.