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miR-29a 通过下调人胃癌中的 p42.3 抑制细胞增殖并诱导细胞周期停滞。

MiR-29a inhibits cell proliferation and induces cell cycle arrest through the downregulation of p42.3 in human gastric cancer.

机构信息

Division of Gastroenterology and Hepatology, Shanghai Jiao-Tong University School of Medicine Renji Hospital, Shanghai Institute of Digestive Disease, Shanghai, China.

出版信息

PLoS One. 2011;6(10):e25872. doi: 10.1371/journal.pone.0025872. Epub 2011 Oct 5.

DOI:10.1371/journal.pone.0025872
PMID:21998710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3187799/
Abstract

As a newly identified and characterized gene, p42.3 is associated with cell proliferation and tumorigenicity. The expression of p42.3 is upregulated in human gastric cancer (GC), but its underlying mechanisms of action are not well understood. MicroRNAs (miRNAs) are known to play vital regulatory roles in many cellular processes. Here we utilized bioinformatics and experimental approaches to investigate the regulatory relationship between miRNAs and the p42.3 gene. We showed that miR-29a could repress p42.3 expression at both the mRNA and protein levels via directly binding to its 3'UTR. Furthermore, an inverse relationship was observed between miR-29a and p42.3 expression in gastric cancer cell lines and GC tissue samples, especially in cases where p42.3 was downregulated. Taken together, we have elucidated previously unrecognized roles of miR-29a and indicated that miR-29a may function, at least partially, by targeting the p42.3 gene in human GC.

摘要

作为一个新鉴定和表征的基因,p42.3 与细胞增殖和致瘤性有关。p42.3 在人类胃癌(GC)中的表达上调,但作用机制尚不清楚。已知 microRNAs(miRNAs)在许多细胞过程中发挥重要的调节作用。在这里,我们利用生物信息学和实验方法研究了 miRNAs 与 p42.3 基因之间的调节关系。我们表明,miR-29a 可以通过直接结合其 3'UTR 在 mRNA 和蛋白质水平上抑制 p42.3 的表达。此外,在胃癌细胞系和 GC 组织样本中观察到 miR-29a 和 p42.3 表达之间存在反相关关系,尤其是在 p42.3 下调的情况下。总之,我们已经阐明了 miR-29a 的以前未被识别的作用,并表明 miR-29a 至少部分通过靶向人类 GC 中的 p42.3 基因发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/90ad8c5e2242/pone.0025872.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/dade273ac01c/pone.0025872.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/a53aa43132fd/pone.0025872.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/0c01448ca9ce/pone.0025872.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/d7b2c145d034/pone.0025872.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/7de633ad1d61/pone.0025872.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/90ad8c5e2242/pone.0025872.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/dade273ac01c/pone.0025872.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/a53aa43132fd/pone.0025872.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/0c01448ca9ce/pone.0025872.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/d7b2c145d034/pone.0025872.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/7de633ad1d61/pone.0025872.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ba0/3187799/90ad8c5e2242/pone.0025872.g006.jpg

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