Table 1.
Targeting molecular mechanisms that support cell autonomous migration.
| Target | Molecular Mechanism | Reference |
|---|---|---|
| Ras/Rho/CDC 42 | Small GTPases involved in the reorganization of actin and microtubulin network formation that controls cell protrusions (lamellipodia and filopodia) | [52] |
| Snail, Twist | Transcription factors that functions as a regulators of the EMT phenotype promote migration and tumor cell motility | [63, 105, 106] |
| SATB1 | Transcriptional regulator (chromatin organizer and transcription factor) that ntegrates higher-order chromatin architecture with gene regulation. Ectopic SATB1 expression promotes aggressive phenotype while its downregulation promotes E-cadherin expression and inhibits the transcription factors Snail and Twist. | [64, 185] |
| Src | A non-receptor tyrosine kinase that transmits integrin-dependent signals central to cell movement and proliferation | [55, 107] |
| WAVE3 | An actin nucleation/polymerizing factor that binds actin and the Arp2/3 complex. It is an effector molecule involved in the transmission of signals form tyrosine kinase receptors and small GTPases to the actin cytoskeleton. Normally expressed in ovary in brain but ectopic expression can occur at high leves in diverse cancers where it promotes motility and metastasis. | [183, 184] |
| miRNA-10b, miR34a | microRNA can regulate expression of a large group of genes that control migration. Both upregulation of migration promoters and down regulation of migration inhibitors has been observed. | [43] [67] |
Molecules included here are representative molecular determinants of the underlying principle