Chenzhang Shi

Obesity and Risk of Colorectal Cancer: A Systematic Review of Prospective Studies

Background Mounting evidence indicates that obesity may be associated with the risk of colorectal cancer (CRC). To conduct a systematic review of prospective studies assessing the association of obesity with the risk of CRC using meta-analysis. Methodology/Principal Findings Relevant studies were identified by a search of MEDLINE and EMBASE databases before January 2012, with no restrictions. We also reviewed reference lists from retrieved articles. We included prospective studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between general obesity [measured using body mass index (BMI)] or central obesity [measured using waist circumference (WC)] and the risk of colorectal, colon, or rectal cancer. Approximately 9, 000, 000 participants from several countries were included in this analysis. 41 studies on general obesity and 13 studies on central obesity were included in the meta-analysis. The pooled RRs of CRC for the obese vs. normal category of BMI were 1.334 (95% CI, 1.253–1.420), and the highest vs. lowest category of WC were 1.455 (95% CI, 1.327–1.596). There was heterogeneity among studies of BMI (P<0.001) but not among studies of WC (P = 0.323). Conclusions Both of general and central obesity were positively associated with the risk of CRC in this meta-analysis.

SP1 mediates the link between methylation of the tumour suppressor miR-149 and outcome in colorectal cancer.

Although recent studies indicate that DNA methylation contributes to the down‐regulation of microRNAs (miRNAs) in colorectal cancer (CRC), this field remains largely unexplored. To identify methylation‐silenced miRNAs and clarify their role in CRC, we performed a microarray analysis and screened for miRNAs that were induced in CRC cells by 5‐aza‐2′‐deoxycytidine treatment or by the knockdown of DNA methyltransferases. The DNA methylation status of the candidate miRNA was analysed by bisulphite sequencing PCR and methylation‐specific PCR. We found that miRNA‐149 (miR‐149) was epigenetically silenced in CRC and down‐regulation of miR‐149 was associated with hypermethylation of the neighbouring CpG island (CGI). Quantitative RT‐PCR analysis demonstrated that the miR‐149 level was markedly reduced in 51.6% of the CRC tissues compared with matched non‐cancerous tissues. In addition, low expression of miR‐149 was associated with a greater depth of invasion (

SP1 mediates the link between methylation of the tumour suppressor miR-149 and outcome in colorectal cancerlSUPg†l/SUPg

\it{p} = 0.012

MicroRNA-21 Knockout Improve the Survival Rate in DSS Induced Fatal Colitis through Protecting against Inflammation and Tissue Injury

), lower 5‐year survival rate (

Elevated oncofoetal miR-17-5p expression regulates colorectal cancer progression by repressing its target gene P130

\it{p} = 0.025

Overexpression of miR-21 in patients with ulcerative colitis impairs intestinal epithelial barrier function through targeting the Rho GTPase RhoB.

), and was found to be an independent prognostic factor for overall survival (

NIRF is frequently upregulated in colorectal cancer and its oncogenicity can be suppressed by let-7a microRNA

\it{p} = 0.016

Cyclin D1 G870A Polymorphism Contributes to Colorectal Cancer Susceptibility: Evidence from a Systematic Review of 22 Case-Control Studies

) in a multivariate analysis. Moreover, transfection of miR‐149 inhibited cell growth and invasion of CRC cells in vitro. We also identified mRNA for Specificity Protein 1 (SP1, Sp1), a potential oncogenic protein, as a target of miR‐149. Our data suggest that, as a methylation‐sensitive miRNA, miR‐149 may play an important role as a tumour suppressor in CRC, which has prognostic and therapeutic implications. Copyright

Involvement of the mannose receptor and p38 mitogen-activated protein kinase signaling pathway of the microdomain of the integral membrane protein after enteropathogenic Escherichia coli infection.

Although recent studies indicate that DNA methylation contributes to the down‐regulation of microRNAs (miRNAs) in colorectal cancer (CRC), this field remains largely unexplored. To identify methylation‐silenced miRNAs and clarify their role in CRC, we performed a microarray analysis and screened for miRNAs that were induced in CRC cells by 5‐aza‐2′‐deoxycytidine treatment or by the knockdown of DNA methyltransferases. The DNA methylation status of the candidate miRNA was analysed by bisulphite sequencing PCR and methylation‐specific PCR. We found that miRNA‐149 (miR‐149) was epigenetically silenced in CRC and down‐regulation of miR‐149 was associated with hypermethylation of the neighbouring CpG island (CGI). Quantitative RT‐PCR analysis demonstrated that the miR‐149 level was markedly reduced in 51.6% of the CRC tissues compared with matched non‐cancerous tissues. In addition, low expression of miR‐149 was associated with a greater depth of invasion (

ACF7 regulates colonic permeability

\it{p} = 0.012