Inhibitory Effect of 5-Aza-2’-Deoxytidine on Cell Viability of the Oral Cancer Cell Line, ORL-48T

 
 
 
  • Abstract
  • Keywords
  • References
  • PDF
  • Abstract


    Oral cancer is recorded as the sixth highest malignancy globally. 5-Aza-2'-deoxycytidine (5-Aza-dC) has been applied as an inhibitory agent in various tumourous cells. Previous studies showed that 5-Aza-dC can inverse genes silencing resulting from hypermethylation process. Inhibitory effects of 5-Aza-dC on oral cancer cell lines, ORL-48T proliferation was studied using 3-(4,5-dimethylthiazol-2-yl)-2,5 -diphenyltetrazolium bromide (MTT)-based assay in this study. The results demonstrated the treatment with 20 µM 5-Aza-dC for 144 h and 40 µM with 72 h respectively, revealed a significantly decreased percentage of viable tumour cells (p= 0.03). This current study provides an evidence of the inhibitive effect of 5-Aza-dC on the ORL-48T cells proliferation.

     

     


  • Keywords


    Oral Cancer; 5-aza-2'-deoxycytidine; MTT Assay; Cell Viability.

  • References


      [1] J. Varshney and S. Subramanian, “Small is the new big – interplay of miRNAs in cancer,” Curr. Sci., vol. 107, no. 5, pp. 803–814, 2014.

      [2] World Health Organisation, “Oral health fact sheet No. 318,” Geneva World Heal. Organ., 2012.

      [3] S. Warnakulasuriya, “Global epidemiology of oral and oropharyngeal cancer,” Oral Oncol., vol. 45, no. 4, pp. 309–316, 2009.

      [4] A. A. Razak, N. Saddki, N. N. Naing, and N. Abdullah, “Oral cancer presentation among Malay patients in hospital Universiti Sains Malaysia, Kelantan,” Asian Pac J Cancer Prev, vol. 10, pp. 1131–1136, 2009.

      [5] R. B. Zain, “Cultural and dietary risk factors of oral cancer and precancer—a brief overview,” Oral Oncol., vol. 37, no. 3, pp. 205–210, 2001.

      [6] W. M. N. Ghani, J. G. Doss, M. Jamaluddin, D. Kamaruzaman, and R. B. Zain, “Oral cancer awareness and its determinants among a selected Malaysian population,” Asian Pacific J. Cancer Prev., vol. 14, no. 3, pp. 1957–1963, 2013.

      [7] J. Goffin and E. Eisenhauer, “DNA methyltransferase inhibitors—state of the art,” Ann. Oncol., vol. 13, no. 11, pp. 1699–1716, 2002.

      [8] D. Mossman, K. Kim, and R. J. Scott, “Demethylation by 5-aza-2 ’-deoxycytidine in colorectal cancer cells targets genomic DNA whilst promoter CpG island methylation persists,” BMC Cancer, vol. 10, p. 366, 2010.

      [9] L. A. Michalowsky and P. A. Jones, “Differential nuclear protein binding to 5-azacytosine-containing DNA as a potential mechanism for 5-aza-2’-deoxycytidine resistance.,” Mol. Cell. Biol., vol. 7, no. 9, pp. 3076–3083, 1987.

      [10] C. Balch et al., “Antimitogenic and chemosensitizing effects of the methylation inhibitor zebularine in ovarian cancer,” Mol. Cancer Ther., vol. 4, no. 10, pp. 1505–1514, 2005.

      [11] A. A. Stepanenko and V. V. Dmitrenko, “Pitfalls of the MTT assay: Direct and off-target effects of inhibitors can result in over/underestimation of cell viability,” Gene, vol. 574, no. 2, pp. 193–203, 2015.

      [12] X. Q. Zhou et al., “Effects of 5-aza-2 9 deoxycytidine on RECK gene expression and tumor invasion in salivary adenoid cystic carcinoma,” Brazilian J. Med. Biol. Res., vol. 48, no. 3, pp. 254–260, 2015.

      [13] L. C. Hsi, X. Xi, Y. Wu, and S. M. Lippman, “The methyltransferase inhibitor 5-aza-2-deoxycytidine induces apoptosis via induction of 15-lipoxygenase-1 in colorectal cancer cells,” Mol Cancer Ther, vol. 4, no. 11, pp. 1740–1746, 2005.

      [14] Y. Tan et al., “Transcriptional inhibiton of Hoxd4 expression by miRNA-10a in human breast cancer cells,” BMC Mol. Biol., vol. 10, no. 1, p. 12, 2009.

      [15] M. Hemberger, R. Udayashankar, P. Tesar, H. Moore, and G. J. Burton, “ELF5-enforced transcriptional networks define an epigenetically regulated trophoblast stem cell compartment in the human placenta,” Hum. Mol. Genet., vol. 19, no. 12, pp. 2456–2467, 2010.

      [16] K. G. Heah, N. R. Shobri, N. A. Khoruddin, S. N. Suhaimi, Y. P. M. Yusof, and T. T. Hock, “A Review on Di Methyl Thiazoldiphenyl-Tetrazoliumbromide (MTT) Assay in Cell Viability,” Res. J. Appl. Sci., vol. 12, no. 7–9, pp. 372–378, 2017.

      [17] T. L. Riss, R. A. Moravec, A. L. Niles, H. A. Benink, T. J. Worzella, and L. Minor, “Cell viability assays,” Assay Guid. Man., 2013.

      [18] X. Cheng, J. Sherman, W. Murphy, E. Ratovitski, J. Canady, and M. Keidar, “The effect of tuning cold plasma composition on glioblastoma cell viability,” PLoS One, vol. 9, no. 5, p. e98652, 2014.

      [19] M. J. Stoddart, “Chapter 1 Cell Viability Assays : Introduction,” vol. 740, pp. 1–6, 2011.

      [20] N. S. Syairah et al., “IC50 OF Ganoderma Lucidum Extract on Oral Cancer Cells, ORL-48T,” J. Fundam. Appl. Sci., vol. 9, no. 6S, pp. 237–245, 2017.


 

View

Download

Article ID: 25699
 
DOI: 10.14419/ijet.v7i4.42.25699




Copyright © 2012-2015 Science Publishing Corporation Inc. All rights reserved.