Table 1.
Transcriptional mechanisms by which Nanotetrac/tetrac is anti-angiogenic.
| Angiogenesis-relevant target | Action | References |
|---|---|---|
| bFGF transcription | ↓ | (18) |
| VEGFA transcription | ↓ | (11, 26) |
| EGFR transcription | ↓ | (34) |
| TSP1 (THBS1) transcription | ↑ | (26, 34) |
| miR-21 transcription | ↓ | (31) |
| miR-15A transcription | ↑ | (31) |
| Cellular bFGF abundance | ↓ | (18) |
| Cellular Ang-2 abundance | ↓ | (22) |
| Cellular MMP-9 abundance | ↓ | (35) |
| Pro-angiogenic activity of thyroid hormone | ↓ | (36) |
Measurements of gene transcription were made in breast cancer (34) and medullary thyroid carcinoma cells (26). Protein abundance decreases are presumed to reflect decreased expression of specific genes. The pro-angiogenic activity of thyroid hormone involves non-transcriptional mechanisms as well as actions on specific gene expression shown in this table. Mechanisms that appear to be non-transcriptional are crosstalk between integrin αvβ3 and adjacent vascular growth factor receptors on the cell surface, cell release mechanisms for newly synthesized growth factors and regulation of endothelial cell motility (11, 18, 36).