Tong-Yi Shen

Proteomics Identification of Desmin as a Potential Oncofetal Diagnostic and Prognostic Biomarker in Colorectal Cancer

Colorectal cancer (CRC) is the third most common cancer worldwide and has poor prognosis. To identify the oncofetal proteins involved in CRC carcinogenesis, differentially expressed proteins among fetal colorectal tissues, CRC, and the paired tumor-adjacent normal colorectal tissues were investigated by a two-dimensional gel electrophoresis and MALDI-TOF/TOF-based proteomics approach. 42 protein spots were differentially expressed among these tissues, and 22 proteins were identified by MS analysis. Desmin and zinc finger protein 829 were found to be elevated in CRC tissue and fetal colorectal tissue compared with normal colorectal tissue. The elevated expression of desmin in CRC tissue and different developmental stages of fetus colon was confirmed by RT-PCR and Western blot analysis. Immunohistochemical analysis showed that the elevated expression of desmin was correlated with the severity and differentiation of CRC and decreased survival rate of CRC patients. Finally by developing a highly sensitive immunoassay, desmin could be detected in human serum and was significantly elevated in CRC patients compared with healthy volunteers. We propose that desmin be considered a potential oncofetal serum tumor marker for CRC that may have significance in the detection of patients with CRC.

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

Heterogeneous nuclear ribonucleoprotein A1 is identified as a potential biomarker for colorectal cancer based on differential proteomics technology.

), lower 5‐year survival rate (

Lactobacillus plantarum ameliorates colonic epithelial barrier dysfunction by modulating the apical junctional complex and PepT1 in IL-10 knockout mice

\it{p} = 0.025

Lactobacillus plantarum surface layer adhesive protein protects intestinal epithelial cells against tight junction injury induced by enteropathogenic Escherichia coli

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

Lactobacillus plantarum inhibits intestinal epithelial barrier dysfunction induced by unconjugated bilirubin.

\it{p} = 0.016

Effects of oral Lactobacillus plantarum on hepatocyte tight junction structure and function in rats with obstructive jaundice.

) 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

Effects of Lactobacillus plantarum on gut barrier function in experimental obstructive jaundice

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 (

Functional characterization of MIMP for its adhesion to the intestinal epithelium.

\it{p} = 0.012