ID1 regulates U87 human cell proliferation and invasion

August 2013
Oncology Letters;2013, Vol. 6 Issue 4, p921
Academic Journal
Despite therapeutic advances, the prognosis of patients diagnosed with malignant glioma has not improved in recent years. In particular, the molecular mechanisms that mediate glioma invasion remain poorly understood. The importance of ID1 in promoting tumor invasion and metastasis has recently emerged and a role for ID1 as a possible molecular marker of tumor aggressiveness has been proposed. To investigate the biological function of ID1 in glioblastomas, ID1-silenced U87 glioblastoma multiforme (GBM) cells were constructed using a small hairpin RNA (shRNA) sequence. The effect of the knockdown of ID1 on proliferation and invasion in these cells was analyzed using the 5-bromo-2'-deoxy-uridine cell proliferation, Transwell invasion, scratch and cell adhesion assays. Compared with the controls, the U87 cells expressing ID1-shRNA exhibited a significantly decreased proliferation and invasion capacity (P<0.05), as well as increased cell adhesion. Furthermore, silencing ID1 reduced the expression of c-Myc, cyclin D1 and β-catenin, while increasing E-cadherin expression in U87 cells. This study showed that ID1 regulates the metastatic potential of GBM cells by controlling the epithelial-mesenchymal transition. Therefore, ID1 is a potential prognostic indicator and therapeutic target in glioblastomas.


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