» Articles » PMID: 25622259

Promoter Hypermethylation of Tumour Suppressor Genes As Potential Biomarkers in Colorectal Cancer

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2015 Jan 27
PMID 25622259
Citations 85
Authors
Affiliations
Soon will be listed here.
Abstract

Colorectal cancer (CRC) is a common malignancy and the fourth leading cause of cancer deaths worldwide. It results from the accumulation of multiple genetic and epigenetic changes leading to the transformation of colon epithelial cells into invasive adenocarcinomas. In CRC, epigenetic changes, in particular promoter CpG island methylation, occur more frequently than genetic mutations. Hypermethylation contributes to carcinogenesis by inducing transcriptional silencing or downregulation of tumour suppressor genes and currently, over 600 candidate hypermethylated genes have been identified. Over the past decade, a deeper understanding of epigenetics coupled with technological advances have hinted at the potential of translating benchtop research into biomarkers for clinical use. DNA methylation represents one of the largest bodies of literature in epigenetics, and hence has the highest potential for minimally invasive biomarker development. Most progress has been made in the development of diagnostic markers and there are currently two, one stool-based and one blood-based, biomarkers that are commercially available for diagnostics. Prognostic and predictive methylation markers are still at their infantile stages.

Citing Articles

Data-Driven Identification of Early Cancer-Associated Genes via Penalized Trans-Dimensional Hidden Markov Models.

Hajebi Khaniki S, Shokoohi F Biomolecules. 2025; 15(2).

PMID: 40001597 PMC: 11853217. DOI: 10.3390/biom15020294.


Nicotinamide mononucleotide protects STAT1 from oxidative stress-induced degradation to prevent colorectal tumorigenesis.

Li T, Luo C, Liu Z, Li J, Han M, Zhang R MedComm (2020). 2024; 5(12):e70006.

PMID: 39575303 PMC: 11581775. DOI: 10.1002/mco2.70006.


Unmasking early colorectal cancer clues: in silico and in vitro investigation of downregulated IGF2, SOCS1, MLH1, and CACNA1G in SSA polyps.

Mirbahari S, Fatemi N, Savabkar S, Chaleshi V, Zali N, Taleghani M Mol Biol Rep. 2024; 51(1):764.

PMID: 38874740 PMC: 11178608. DOI: 10.1007/s11033-024-09683-3.


Colorectal cancer microbiome programs DNA methylation of host cells by affecting methyl donor metabolism.

Liu Z, Zhang Q, Zhang H, Yi Z, Ma H, Wang X Genome Med. 2024; 16(1):77.

PMID: 38840170 PMC: 11151592. DOI: 10.1186/s13073-024-01344-1.


Associations in cell type-specific hydroxymethylation and transcriptional alterations of pediatric central nervous system tumors.

Lee M, Azizgolshani N, Zhang Z, Perreard L, Kolling F, Nguyen L Nat Commun. 2024; 15(1):3635.

PMID: 38688903 PMC: 11061294. DOI: 10.1038/s41467-024-47943-9.


References
1.
Issa J . CpG island methylator phenotype in cancer. Nat Rev Cancer. 2004; 4(12):988-93. DOI: 10.1038/nrc1507. View

2.
Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M . Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2014; 136(5):E359-86. DOI: 10.1002/ijc.29210. View

3.
Song B, Jain S, Lin S, Chen Q, Block T, Song W . Detection of hypermethylated vimentin in urine of patients with colorectal cancer. J Mol Diagn. 2012; 14(2):112-9. PMC: 3349838. DOI: 10.1016/j.jmoldx.2011.12.003. View

4.
Liang G, Salem C, Yu M, Nguyen H, Gonzales F, Nguyen T . DNA methylation differences associated with tumor tissues identified by genome scanning analysis. Genomics. 1998; 53(3):260-8. DOI: 10.1006/geno.1998.5502. View

5.
Zou H, Harrington J, Shire A, Rego R, Wang L, Campbell M . Highly methylated genes in colorectal neoplasia: implications for screening. Cancer Epidemiol Biomarkers Prev. 2007; 16(12):2686-96. DOI: 10.1158/1055-9965.EPI-07-0518. View