Furthermore, we showed that p27(Kip1) was an important regulator downstream of CCND3 and that the accumulation of p27(Kip1) in the cytoplasm might be responsible for the miR-195-mediated cell invasion inhibition in glioblastoma cells.
Since over-expression of the ccnd3 gene, but not the H40682 locus, was detected in the cell line CCF-STTG1, the increased amounts of cyclin D3 caused by gene amplification could be involved in the development and/or progression of this glioblastoma.
Amplification and overexpression of the CCND3 gene was detected in the glioblastoma cell line CCF-STTG1, as well as in one primary glioblastoma and in the sarcomatous component of one gliosarcoma.