<b>Purpose:</b> Loss of cell-cycle control is a hallmark of cancer, which can be targeted with agents, including cyclin-dependent kinase-4/6 (CDK4/6) kinase inhibitors that impinge upon the G<sub>1</sub>-S cell-cycle checkpoint via maintaining activity of the retinoblastoma tumor suppressor (RB).
<b>Results</b>: We found that miR-665 was markedly reduced in RB tissues and cell lines and that lower miR-665 expression was strongly associated with tumor size, TNM stage, and differentiation in patients with RB.
1734-1745) found high levels of the miR-17~92 and miR-106b-25 microRNAs in primary retinoblastomas and show that overexpression of miR-17~92 accelerates retinoblastoma development in mice by promoting proliferation, in part by reducing expression of the cell cycle inhibitor p21.
2) The positive expression rate of PlGF proteins in RB was 73.8%, which was higher in tumors with optic nerve invasion than in tumors without the invasion; the expression was significantly different (p=0.001).
3) The expression of claudin-1 in RB was negatively correlated with the presence of choroidal invasion (r=0.52, p≤0.0001) and optic nerve infiltration (r=0.49, p=0.0003).
3) The expression of claudin-1 in RB was negatively correlated with the presence of choroidal invasion (r=0.52, p≤0.0001) and optic nerve infiltration (r=0.49, p=0.0003).
Retinoblastoma (Rb) tumor suppressor genes' products and of the proteins regulating its phosphorylation and function in G1 arrest, p16INK4A and cyclin D1, play important roles in the regulation of the cell cycle.
Retinoblastoma (Rb) tumor suppressor genes' products and of the proteins regulating its phosphorylation and function in G1 arrest, p16INK4A and cyclin D1, play important roles in the regulation of the cell cycle.