Evidence of increased Id‐1 expression and its role in cell proliferation in nasopharyngeal carcinoma cells

Publisher Website
Google Scholar
Abstract
Inhibitor of differentiation or DNA binding (Id‐1), a helix‐loop‐helix transcription factor, has recently been shown to inactivate the retinoblastoma (RB)/p16INK4a pathway through down‐regulation of p16INK4a and increasing phosphorylation of RB in certain cell types. Nasopharyngeal carcinoma (NPC) is a common cancer in Hong Kong, and inactivation of the tumor suppressor RB at transcription level is a rare event in NPC. The objective of this study was to investigate the role of Id‐1 in NPC cell proliferation and its expression in NPC samples. An NPC cell line, CNE1, was transfected with a retroviral vector containing a full‐length Id‐1 cDNA, and six stable transfectant clones were isolated with differential Id‐1 expression levels. The effect of ectopic Id‐1 expression on serum‐independent cell growth, cell‐cycle distribution, and expression of proteins associated with RB pathway was studied. The Id‐1 expression in five NPC samples was also investigated using immunohistochemistry. Ectopic Id‐1 expression in CNE1 cells resulted in an increase in serum‐independent cell growth, percentage of cells in S phase, and phosphorylation of RB and cyclin‐dependent kinase 2 proteins. In addition, immunohistochemical studies on NPC samples showed that expression of Id‐1 was present in NPC cells but absent in normal tissues. This study demonstrates that Id‐1 plays an important role in cell proliferation in NPC cells, and our results provide evidence for the first time of the significance of Id‐1 expression in NPC cells and suggest a possible role of Id‐1 expression in the inactivation of RB and development of NPC.