MicroRNA-142-3p is frequently upregulated in colorectal cancer and may be involved in the regulation

来源 :Chinese Science Bulletin | 被引量 : 0次 | 上传用户:wlxingyun
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MicroRNAs are small single-stranded RNA molecules consisting of approximately 22 nucleotides (nt), and have post-transcriptional regulatory functions. By gene chip screening, we previously showed that miR-142-3p was significantly upregulated in colorectal cancer tissue and was associated with clinicopathological features, compared with matched non-tumor tissue. In this study, we confirmed significant upregulation of miR-142-3p in 60 colorectal cancer samples and three colorectal cancer cell lines by quantitative real-time PCR (qRT-PCR). Using software and network resources, we predicted TCF7 as a target of miR-142-3p, which we confirmed with dual-luciferase assays. By RT-PCR and Western blot analysis, we found miR-142-3p negatively regulates TCF7 expression post-transcriptionally. CCK8 assays and growth curves indicated that overexpression of miR-142-3p in SW480 colorectal cancer cells potently inhibited cell proliferation in vitro. The expression of TCF7 mRNA and protein was upregulated in both colorectal cancer tissues and colorectal cancer cell lines, closely correlating with its function as an oncogene in promoting tumor cell proliferation and inhibiting apoptosis. With TCF7 as a direct target, our results suggested that miR-142-3p may be involved in the regulation of cell proliferation in colorectal cancer. MicroRNAs are small single-stranded RNA molecules consisting of approximately 22 nucleotides (nt), and have post-transcriptional regulatory functions. By gene chip screening, we previously showed that miR-142-3p was significantly upregulated in colorectal cancer tissue and was associated with clinicopathological features, compared with matched non-tumor tissue. In this study, we confirmed significant upregulation of miR-142-3p in 60 colorectal cancer samples and three colorectal cancer cell lines by quantitative real-time PCR (qRT-PCR). and network resources, we predicted TCF7 as a target of miR-142-3p, which we confirmed with dual-luciferase assays. By RT-PCR and Western blot analysis, we found that miR-142-3p negatively regulates TCF7 expression post-transcriptionally. CCK8 assays and growth curves indicated that overexpression of miR-142-3p in SW480 colorectal cancer cells potently inhibited cell proliferation in vitro. The expression of TCF7 mRNA and protein was upregulat ed in both colorectal cancer tissues and colorectal cancer cell lines, closely correlating with its function as an oncogene in promoting tumor cell proliferation and inhibiting apoptosis. With TCF7 as a direct target, our results suggested that miR-142-3p may be involved in the regulation of cell proliferation in colorectal cancer.
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