Pyrex Journal of Biomedical Research (PJBR)

December 2016 Vol. 2(6), pp. 41-47

ISSN: 2985-8852

Copyright © 2016 Pyrex Journals

Full Length Research Paper

Hypermethylated promoter profiles for tumour supressor APC, p53, MSH6 and MGMT genes in CRC tumours

Ebru Sik1, Ozturk Ozdemir1,2*, Hande Kucuk Kurtulgan2, Mine Urfali1, Metin Sen3, Fatma Silan1

1Department of Medical Genetics, Faculty of Medicine, Canakkale Onsekiz Mart University 17100, Canakkale –Turkey.
2Department of Medical Genetics, Faculty of Medicine, Cumhuriyet University 58140, Sivas-Turkey.
3Department of Medical Genetics, Faculty of Medicine, Cumhuriyet University 58140, Sivas-Turkey.

Corresponding Author E-mail:

Accepted 20th December, 2016


Background and Aim: Colorectal cancer (CRC) results from a multiple steps of genetic and epigenetic parameters that transform a normal cell into cancerous epithelium. Aberrant DNA methylation is a common epigenomic alteration in carcinogenesis. In the present study was aimed to investigate the possible DNA hypomethylation in three candidate tumour supressor (TS) genes in CRC tumours. Method: Twenty CRC solid tumours were analyzed in the current project by epigenetical profilling of target TS genes. Promoter methylation status was evaluated by MS-MLPA technique in current twenty CRC tumours for target p53, MLH6 and MGMT genes. Results: Results showed alterated methylation profiles for p53, MLH6 and MGMT genes in the current CRC tumours. Increased hypermethylation (HM) at different levels were detected all TS genes that examined in the current results. The HM percentages were; APC (20/100%), p53 (12/60%), MSH6 (12/60%) and MGMT (2/10%) respectivelly. No hypermethlation was detected for both BRCA 1-2 (control) genes in all tumoural samples that examined in the current results. Conclusions: Preliminary results from the current project suggest that altered DNA methylation status takes crucial role in CRC initiation and/or progression. Results need to confirm by large-scale of tumoural samples.

Keywords: CRC tumours, promoter hypermethlation, p53, MSH6, MGMT, MS-MLPA technique, epigenetic alteration.

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