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首页> 外文期刊>Journal of Cellular Physiology >MicroRNA-200b stimulates tumour growth in TGFBR2-null colorectal cancers by negatively regulating p27/kip1
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MicroRNA-200b stimulates tumour growth in TGFBR2-null colorectal cancers by negatively regulating p27/kip1

机译：微rna - 200 b刺激肿瘤生长由消极TGFBR2-null结肠直肠癌调节p27 / kip1

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Colorectal cancer (CRC) remains the most common malignancy worldwide. TGF-β1 is often overexpressed in late stages of colorectal carcinogenesis and promotes tumour growth and metastasis. Several reports have verified that the loss of functional TGFBRII expression contributed to escape the tumour suppressor activity of TGF-β1 and that the epithelial-to-mesenchymal transition (EMT) responded to TGF-β1 involved in tumour invasion and metastasis. However, the mechanisms by which TGF-β1 confers a growth advantage to TGFBRII-null colorectal cancer cells have not been elucidated. MicroRNAs (miRNAs) are post-transcriptional inhibitory regulators of gene expression that act by directly binding complementary mRNA and are key determinants of cancer initiation and progression. In this study, we revealed a role for miR-200b in colorectal cancer. MiR-200b was highly expressed in TGFBRII-null tumour tissues and colorectal cancer cell lines and positively correlated with cell proliferation in tumour tissues and cell lines. In contrast, decreasing the miR-200b level in TGFBRII-null cells suppressed cell proliferation and cell cycle progression. Furthermore, in vivo studies also suggested a stimulating effect of miR-200b on TGFBRII-null cell-derived xenografts. CDKN1B (p27/kip1) and RND3 (RhoE) have miR-200b binding sequences within their 3′ untranslated regions and were confirmed to be direct targets of miR-200b using fluorescent reporter assays. Meanwhile, CDKN1B (p27/kip1) played a role in miR-200b-stimulated TGFBR-null CRC. This study suggests that miR-200b plays a tumour-promoting role by targeting CDKN1B (p27/kip1) in CRCs. J. Cell. Physiol. 229: 772-782, 2014.
机译：结直肠癌(CRC)是最常见的全球恶性肿瘤。在晚期结直肠致癌作用和促进肿瘤生长转移。功能的丧失TGFBRII表达式导致逃避肿瘤抑制基因活动的TGF -β1和epithelial-to-mesenchymal过渡(EMT)回应TGF -β1参与肿瘤入侵和转移。TGF -β1赋予TGFBRII-null生长优势结直肠癌细胞尚未阐明。小分子核糖核酸(microrna)转录后抑制管理者行为的基因表达互补的信使rna,通过直接绑定癌症引发的关键决定因素进展。在结直肠癌mir - 200 b。TGFBRII-null肿瘤组织中高度表达结直肠癌细胞系和积极与肿瘤细胞增殖组织和细胞系。mir - 200 b水平TGFBRII-null细胞抑制细胞增殖和细胞周期进展。建议mir - 200 b的刺激效应TGFBRII-null细胞衍生异种移植。(p27 / kip1)和RND3 mir - 200 b (RhoE)绑定序列在其3 '非翻译区和被证实的直接目标使用荧光记者化验mir - 200 b。与此同时,CDKN1B (p27 / kip1)扮演了一个角色mir - 200 - b - TGFBR-null CRC刺激。表明,mir - 200 b扮演一个异变角色通过瞄准CDKN1B crc (p27 / kip1)。细胞。

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