Figure 6

Schematic diagram of MT1G as a tumor suppressor in thyroid cancer cells through regulating the PI3K/Akt and Rb/E2F pathways. MT1G restoration inhibited phosphorylation of Akt, leading to inhibition of cell growth. MT1G decreased Mdm2 expression through inhibiting the activity of Akt kinases. MT1G increased the stability of p53 and E-cadherin by the decreased ubiquitination of Mdm2, contributing to induction of cell cycle arrest and apoptosis and suppression of cell migration and invasion. MT1G also influenced cell growth, such as cell cycle progression and cell death, through inhibiting phosphorylation of Rb.