摘要
AIM: To investigate the copy number variation of NACO3 gene in colorectal cancer (CRC) and its correlation with tumor progression. METHODS: A total of 142 samples of case-matched CRC tissues and adjacent normal tissues were obtained from patients undergoing bowel resection. Quantitative real-time polymerase chain reaction method was used to investigate the copy number variations of NCOA3 as well as gene expression in the collected tissues. RESULTS: Copy number gains of NCOA3 were detected in 39 CRC samples (27.5%) and were correlatedwith tumor progression (χ2 = 6.42, P = 0.0112). Moreover, there was a positive correlation between copy number gain and mRNA over-expression of NCOA3 in CRCs (P = 0.0023). Expression level of NCOA3 mRNA was also enhanced in the CRC samples with unaltered copy numbers (3.85 ± 1.23 vs 2.71 ± 0.64, P < 0.01). CONCLUSION: Sporadic colorectal cancers exhibit different mechanisms of NCOA3 regulation.
AIM： To investigate the copy number variation of NACO3 gene in colorectal cancer （CRC） and its correlation with tumor progression. METHODS： A total of 142 samples of case-matched CRC tissues and adjacent normal tissues were obtained from patients undergoing bowel resection. Quantitative real-time polymerase chain reaction method was used to investigate the copy number variations of NCOA3 as well as gene expression in the collected tissues. RESULTS： Copy number gains of NCOA3 were detected in 39 CRC samples （27.5%） and were correlatedwith tumor progression （χ2 = 6.42, P = 0.0112）. Moreover, there was a positive correlation between copy number gain and mRNA over-expression of NCOA3 in CRCs （P = 0.0023）. Expression level of NCOA3 mRNA was also enhanced in the CRC samples with unaltered copy numbers （3.85 ± 1.23 vs 2.71 ± 0.64, P 〈 0.01）. CONCLUSION： Sporadic colorectal cancers exhibit different mechanisms of NCOA3 regulation.
基金
Supported by Fundamental Research Plan of Shenzhen City, No. JC201005260215A
