DNA Methylation and Colorectal Cancer

Ashktorab, Hassan; Brim, Hassan

doi:10.1007/s11888-014-0245-2

Cited by 51 publications

(34 citation statements)

References 47 publications

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“…In the genome of untransformed cells, approximately 90% of all promoters are unmethylated 12 . The DNA methylation of many genes and their significance in CRC have also been described 13 . The aberrant methylation of CpG islands within gene promoters and first exonic or intronic regions may induce the transcriptional repression of tumor-suppressor genes.…”

Section: Dna Methylation and Crcmentioning

confidence: 99%

DNA methylation assay for colorectal carcinoma

Chen¹,

Wang

Chen

2017

Cancer Biology &Amp; Medicine

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Colorectal carcinoma (CRC) is a common cause of morbidity and mortality worldwide. Two pathogenic pathways are involved in the development of adenoma to CRC. The first pathway involvesAPC/β-catenin characterized by chromosomal instability resulting in the accumulation of mutations. The second pathway is characterized by lesions inDNA mismatch repair genes. Aberrant DNA methylation in selected gene promoters has emerged as a new epigenetic pathway in CRC development. CRC screening is the most efficient strategy to reduce death. Specific DNA methylation events occur in multistep carcinogenesis. Epigenetic gene silencing is a causative factor of CRC development. DNA methylations have been extensively examined in stool from CRC and precursor lesions. Many methylated genes have been described in CRC and adenoma, although no definite DNA methylation biomarkers panel has been established. Multiple DNA methylation biomarkers, including secreted frizzled-related protein 2, secreted frizzled-related protein 1, tissue factor pathway inhibitor 2, vimentin, and methylguanine DNA methyltransferase, have been further investigated, and observations have revealed that DNA methylation biomarkers exhibit with high sensitivity and specificity. These markers may also be used to diagnose CRC and adenoma in early stages. Real time polymerase chain reaction (qPCR) is sensitive, scalable, specific, reliable, time saving, and cost effective. Stool exfoliated markers provide advantages, including sensitivity and specificity. A stool qPCR methylation test may also be an enhanced tool for CRC and adenoma screening.

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Section: Dna Methylation and Crcmentioning

confidence: 99%

DNA methylation assay for colorectal carcinoma

Chen¹,

Wang

Chen

2017

Cancer Biology &Amp; Medicine

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“…Epigenetic mechanisms primarily include modifications to histones, expression of non-coding RNA such as microRNA (miRNA), and variation in DNA methylation [54–57]. Unlike genetic polymorphisms, the influence of epigenetic changes on protein expression is potentially reversible and, thus, may have potential as a colorectal cancer prevention target.…”

Section: Observational Studies On Physical Activity and Colorectal Nementioning

confidence: 99%

“…Unlike genetic polymorphisms, the influence of epigenetic changes on protein expression is potentially reversible and, thus, may have potential as a colorectal cancer prevention target. Molecular epidemiology has identified several target genes that are differentially methylated in normal versus neoplastic colonic epithelium [15, 55, 57]. Gene targets associated with methylation in colorectal cancer include, but are not limited to, MutL homologue 1 ( MLH1 ), adenomatous polyposis coli ( APC ), the cyclin-dependent kinase inhibitor p16 , tumor growth factor beta ( TGF-β ), B-Raf ( BRAF ), and K-Ras ( KRAS ) [15, 55].…”

Section: Observational Studies On Physical Activity and Colorectal Nementioning

confidence: 99%

“…Furthermore, the cytosine–phosphate–guanine (CpG) island methylator phenotype (CIMP) is associated with hypermethylation of CpG islands specifically near promoter regions of genes, including many of those listed above, and it is believed that 30–50 % of colorectal tumors fall into the CIMP category [58]. There is significant evidence for CIMP or methylation at other CpG loci in colorectal cancer etiology [15, 55, 57, 59]. However, few studies have evaluated the influence of physical activity on CIMP or other epigenetic genetic changes in colorectal carcinogenesis.…”

Section: Observational Studies On Physical Activity and Colorectal Nementioning

confidence: 99%

“…The majority of studies related to physical activity and epigenetics evaluate variation in patterns of DNA methylation at CpG sites within genes with known or hypothesized biological function [57, 59]. Global methylation status, or a quantification of total changes across the genome, which, in combination with changes to methylation status at specific loci, are common methods used to evaluate the epigenetic effects of health behaviors [54, 60].…”

Section: Observational Studies On Physical Activity and Colorectal Nementioning

confidence: 99%

See 2 more Smart Citations

Epigenetics and Colorectal Neoplasia: the Evidence for Physical Activity and Sedentary Behavior

Hibler

2015

Curr Colorectal Cancer Rep

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Studies demonstrate that regular physical activity and, more recently, limited sedentary behavior are associated with reduced risk of colorectal neoplasia. However, the biological mechanisms of action for physical activity versus sedentary behavior are not clear. Epigenetic variation is suggested as a potential mechanism that would allow for independent, or possibly even synergistic, effects of activity and inactivity on colorectal epithelium. We describe the evidence for epigenetic variation as a link between physical activity and sedentary behavior in colorectal neoplasia risk. There are few studies that directly evaluate this relationship. However, the growing literature describes a variety of gene targets influenced by activity that are also important to colorectal neoplasia etiology. Future studies may identify epigenetic markers with translational significance in identifying high-risk individuals or those for whom a personalized activity regimen could significantly alter the methylation signature in colon epithelial cells, and thus future risk of colorectal cancer.

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Regulatory effects of lncRNA ATB targeting miR‐200c on proliferation and apoptosis of colorectal cancer cells

Gao

Zhou

Wang

et al. 2019

J of Cellular Biochemistry

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This investigation was intended to elucidate whether long noncoding RNA (lncRNA)‐activated by transforming growth factor‐β (ATB) interacting with miR‐200c could mediate colorectal cancer (CRC) progression, offering potential strategies for diagnosing and treating CRC. Here totally 315 patients with CRC were recruited, and their CRC tissues and adjacent normal tissues were gathered. Concurrently, four colon cancer cell lines (ie, SW620, Lovo, HCT116, and SW480) and the human colon mucosal epithelial cell line (NCM460) were also purchased. Moreover, si‐ATB, si‐NC, miR‐200c mimic, miR‐200c inhibitor, and miR‐NC were prepared for transfection into the CRC cells, and their effects on CRC cell lines were evaluated based on the conduction of 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, colony formation assay, and flow cytometry assay. Eventually, the Luciferase reporter gene assay was carried out to judge if there existed a targeted relationship between ATB and miR‐200c. The results of Cox regression analyses suggested that overexpressed lncRNA ATB, underexpressed miR‐200c, poor tumor differentiation, lymph‐vascular invasion, and perineural invasion were symbolic of shortened survival of the patients with CRC (all P < .05). Besides, transfection of pcDNA3.1‐ATB and miR‐200c inhibitor could boost the viability and proliferation of Lovo and SW620 cell lines (all P < .05). Meanwhile, the expressions of p53 and p21 were also reduced under treatments of pcDNA3.1‐ATB and miR‐200c inhibitor (P < .05). In addition, CDK2 seemed to reverse the contribution of miR‐200c to intensifying viability and proliferation of Lovo and SW420 cell lines (P < .05). Furthermore, ATB might downregulate miR‐200c expression by targeting it (P < .05), and CDK2 was subjected to dual regulation of both ATB and miR‐200c (P < .05). In conclusion, the lncRNA ATB/miR‐200c/CDK2 signaling was responsible for intensified proliferation and prohibited apoptosis of CRC cells, which might provide effective approaches for diagnosing and treating CRC.

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DNA Methylation and Colorectal Cancer

Cited by 51 publications

References 47 publications

DNA methylation assay for colorectal carcinoma

DNA methylation assay for colorectal carcinoma

Epigenetics and Colorectal Neoplasia: the Evidence for Physical Activity and Sedentary Behavior

Regulatory effects of lncRNA ATB targeting miR‐200c on proliferation and apoptosis of colorectal cancer cells

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