Downregulation of MTA-1, complex of CDK2–cyclin E, and NF-kB expressions as a molecular target therapy of oral Burkitt’s lymphoma cells mediated by sense KIP-1 and antisense SKP-2

Abstract

Aim: To examine the decreased of metastatic associated protein-1 (MTA-1), complex of cyclin-dependent kinase-2 (CDK2)–cyclin E, and nuclear factor-kappa beta (NF-kB) expression as a molecular target therapy of oral Burkitt’s lymphoma (Raji) cells mediated by oligonucleotides KIP-1 sense (KIP-1 S) and SKP-2 antisense (SKP-2 AS). Materials and Methods: In the study, the pure laboratory experimental with posttest only control group design was confirmed. The MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] assay was performed to evaluate the suppression of cell growth. The chemotactic migration activity was carried out by Boyden chamber assay. Activation of MTA-1, NF-kB, cyclin E, CDK2, SKP-2, KIP-1, and α-tubulin was investigated by Western blot analysis. Apoptosis cells were analyzed by caspase-3 and caspase-9. Results: The growth inhibition and chemotactic migration activity of KIP-1 S and SKP-2 AS cells were significantly inhibited when compared with the scrambled control (SC) cells. Interestingly, Raji-KIP-1 S has potentially greater cell growth and migrated chemotactic suppression than SKP-2 AS. Induction of cell apoptosis was confirmed in KIP-1 S and SKP-2 AS proofed by increasing the activation of caspase-3 and caspase-9. Decreased level of MTA-1, NF-kB, cyclin E, CDK2, SKP-2, and increased level of KIP-1 protein were detected in KIP-1 S- and SKP-2 AS-treated cells. Conclusion: KIP-1 S and SKP-2 AS have strong antitumor activity on the oral Burkitt’s lymphoma cells through downregulation of MTA-1, CDK2–cyclin E complex, and NF-kB expression. However, KIP-1 S had a stronger antitumor activity than SKP-2 AS targeting these molecules could represent a promising new therapeutic approach for this type of tumor.