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Research Paper | Medicine Science | Indonesia | Volume 4 Issue 12, December 2015
Up-Regulation of S-Phase Kinase Associated Protein-2 Antisense Induces Cell Growth and Migration Chemotactic Suppression and Apoptosis in a Malignant Oral Burkitts Lymphoma Cells
Supriatno  | Sartari Entin Yuletnawati 
Abstract: Burkitts lymphoma (BL) is an uncommon type of Non-Hodgkin lymphoma (NHL). It is a highly aggressive type of B-cell lymphoma and the most common childhood cancer. Treatment for this cancer is still limited. However, a new strategy for refractory tumor, gene therapy is watched with keen interest. One of method for high-efficiency and region-controlled in vitro gene transfer was developed by antisense oligonucleotide. In the present study, Skp2 sense (p45Skp2 S), Skp2 antisense (p45Skp2 AS) and Skp2 neo (empty vector) were transfected into an oral Burkitts lymphoma (Raji) cell line. The aim of study was to examine the Skp2 AS up-regulation toward the cell growth and migration chemotatic suppression and apoptosis induction in an oral Burkitts lymphoma cells in vitro. The efficiency of Skp2 S and Skp2 AS gene transfection in cell growth inhibition test was confirmed by MTT [3- (4, 5-dimethythiazol-2-yl) -2, 5-diphenyltetrazolium bromide] assay. To estimate the suppression of chemotatic migration cell was examined by Boyden chamber assay and cell growth test. Furthermore, colorimetric assay caspase-3 and caspase-9 were used to know the apoptosis induction. Results revealed the Raji cell growth and migration chemotatic were markedly suppressed by Skp2 AS. Skp2 AS-treated cell induced apoptosis characterized by an increase caspase-3 and -9 proteolytic activities. These results suggest that up-regulated of Skp 2 AS appear to induce cell growth and migration chemotatic suppression and apoptosis induction in Raji cells targeting this molecule could represent a promising new therapeutic approach for this type of tumor.
Keywords: cell growth, Skp2 AS, Burkitts lymphoma cell, apoptosis, migration
Edition: Volume 4 Issue 12, December 2015,
Pages: 1639 - 1644
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