Abstract
Recent studies revealed that Musashi-1and beta1-integrin were putative stem cell genes. Overexpressions of Musashi-1 and beta1-integrin have been reported in some tumor tissues and cell lines. This study was to detect expressions of the two genes in colorectal adenomas and carcinomas and to analyze the correlation between Musashi-1 and beta1-integrin. Musashi-1 and beta1-integrin immunoreactivity was studied immunohistochemically in tissue microarray-based samples containing 69 colorectal adenocarcinomas, eight normal mucosa, and eight adenomas, and their messenger RNA (mRNA) expression level was detected by RT-PCR in resected specimens including the three types of tissue. A percentage of 66.7% (46/69) and 59.2% (41/69) of colorectal adenocarcinomas were immunoreactive with Musashi-1 and beta1-integrin, respectively. The expressions of Musashi-1 and beta1-integrin protein were significantly higher in tissue samples of stage III than those of stage I-II (P = 0.0252; P = 0.0018, respectively). beta1-integrin expression was higher in group of adenocarcinomas than that of adenomas (P = 0.0276). Musashi-1 expression was closely correlated with beta1-integrin (rs = 0.631, P = 0.0001). Significant differences of Musashi-1 and beta1-integrin mRNA expression levels were found between the normal colorectal mucosa, adenoma, and adenocarcinoma tissues (P = 0.01; P = 0.03, respectively). Musashi-1 and beta1-integrin may be involved in human colorectal tumor carcinogenesis and progression. Our observations also indicate the need for further investigations to test in vivo whether cells with these markers have stem cell properties.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
