MiR-26b是前列腺癌中的抑癌微RNA（英文）

发布时间：2018-05-27 23:34

  本文选题：miR-b + 前列腺癌细胞　； 参考：《生物化学与生物物理进展》2017年06期

【摘要】：微RNAs(又称miRNAs或miRs)是一类长度为19~24个核苷酸的单链非编码RNA分子.miRNA通过与其靶向的mRNA分子序列特异性互补配对,调节mRNA表达水平,抑制转录后的蛋白质翻译.miRNA在肿瘤中既可作为致癌因子也可作为抑癌因子.本研究前期已报道miR-26b在前列腺癌细胞系中低表达,并且抑制细胞自噬.本研究进一步全面揭示miR-26b对前列腺肿瘤细胞的作用.我们发现过表达miR-26b能够在体外抑制前列腺癌细胞的增殖和侵袭,并抑制裸鼠体内原位异种前列腺肿瘤的生长.为了探究miR-26b对前列腺癌细胞增殖和侵袭的潜在调控机制,我们进行了表达谱芯片鉴定miR-26b调控基因.表达谱芯片分析表明,在前列腺癌细胞系PC-3中过表达miR-26b后,显著上调的基因57个,显著下调的基因55个(变化倍数均大于2,且P值小于0.05).差异基因的功能多与细胞增殖、凋亡调控、蛋白质磷酸化和泛素化修饰调控过程相关,并且富集在多种信号通路中,例如TNF和TGF-β信号通路.在这些筛选出的基因中,CEACAM6表达水平下调2.17倍;序列分析及实验验证表明,CEACAM6的3′UTR区存在miR-26b的互补序列,是miR-26b的直接靶标.本研究证明了miR-26b能够靶向结合抑制CEACAM6的表达,从而抑制前列腺癌细胞在体外和体内的细胞增殖和侵袭活性,miR-26b是前列腺癌中的抑癌microRNA.
[Abstract]:MicroRNas (also known as miRNAs or miRs) are a class of single-stranded non-coding RNA molecules with a length of 19~ 24 nucleotides. MiRNAs regulate the expression level of mRNA by specific complementary pairing with their targeted mRNA molecules. Inhibition of post-transcriptional protein translation. MiRNA can be used as both carcinogen and tumor suppressor in tumor. This study reported that miR-26b was expressed in prostate cancer cells and inhibited autophagy. This study further revealed the effect of miR-26b on prostate tumor cells. We found that overexpression of miR-26b could inhibit the proliferation and invasion of prostate cancer cells in vitro and inhibit the growth of xenogeneic prostate neoplasms in vivo in nude mice. In order to investigate the potential regulatory mechanism of miR-26b on the proliferation and invasion of prostate cancer cells, we identified the miR-26b regulatory gene by expression microarray. Expression microarray analysis showed that after overexpression of miR-26b in prostate cancer cell line PC-3, 57 genes were significantly up-regulated and 55 genes were significantly down-regulated (change times were more than 2, P < 0.05). The function of differentially expressed genes is closely related to cell proliferation, apoptosis, protein phosphorylation and ubiquitin modification, and is enriched in many signal pathways, such as TNF and TGF- 尾 signaling pathways. The expression level of CEACAM6 was down-regulated by 2.17 times in these selected genes, and the sequence analysis and experimental verification showed that the 3'UTR region of CEACAM6 contained complementary miR-26b sequence, which was the direct target of miR-26b. This study demonstrated that miR-26b can target to inhibit the expression of CEACAM6 and thus inhibit the cell proliferation and invasion activity of prostate cancer cells in vitro and in vivo.
【作者单位】： 西北农林科技大学生命科学学院;Faculty
【基金】：supported by grants from National Instrumentation Program(2012YQ030261) The National Natural Science Foundation of China(31540002,31571194) Northwest A&F University Doctoral Scientific Research Fund(Z109021633)~~
【分类号】：R737.25
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本文编号：1944272