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miR-148a 通过靶向胃癌细胞中的 p27 促进细胞增殖。

miR-148a promoted cell proliferation by targeting p27 in gastric cancer cells.

机构信息

State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing, PR China.

出版信息

Int J Biol Sci. 2011 May 5;7(5):567-74. doi: 10.7150/ijbs.7.567.

DOI:10.7150/ijbs.7.567
PMID:21552422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3088878/
Abstract

Accumulating evidence has shown that miRNAs are aberrantly expressed in human gastric cancer and crucial to tumorigenesis. Herein, we identified the role of miR-148a in gastric cell proliferation. miR-148a knockdown inhibited cell proliferation in gastric cancer cell lines. Conversely, miR-148a overexpression promoted cell proliferation and cell cycle progression. p27, a key inhibitor of cell cycle, was verified as the target of miR-148a, indicating miR-148a might downregulate p27 expression to promote gastric cell proliferation. Moreover, we confirmed that miR-148a expression was frequently and dramatically downregulated in human advanced gastric cancer tissues, and observed a good inverse correlation between miR-148a and p27 expression in tumor samples. Thus, our results demonstrated that miR-148a downregulation might exert some sort of antagonistic function in cell proliferation, rather than promote cell proliferation in gastric cancer.

摘要

越来越多的证据表明,miRNAs 在人类胃癌中表达异常,对肿瘤发生至关重要。在此,我们确定了 miR-148a 在胃细胞增殖中的作用。miR-148a 敲低抑制胃癌细胞系中的细胞增殖。相反,miR-148a 过表达促进细胞增殖和细胞周期进程。p27 是细胞周期的关键抑制剂,被验证为 miR-148a 的靶标,表明 miR-148a 可能下调 p27 的表达以促进胃细胞增殖。此外,我们证实 miR-148a 在人类晚期胃癌组织中频繁且显著下调,并在肿瘤样本中观察到 miR-148a 与 p27 表达之间存在良好的负相关关系。因此,我们的结果表明,miR-148a 的下调可能在细胞增殖中发挥某种拮抗作用,而不是促进胃癌中的细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/0616ccfd0366/ijbsv07p0567g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/e993b92d897d/ijbsv07p0567g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/819d756960ac/ijbsv07p0567g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/695d997f8db5/ijbsv07p0567g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/05987c13e8d2/ijbsv07p0567g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/0616ccfd0366/ijbsv07p0567g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/e993b92d897d/ijbsv07p0567g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/819d756960ac/ijbsv07p0567g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/695d997f8db5/ijbsv07p0567g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/05987c13e8d2/ijbsv07p0567g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c13/3088878/0616ccfd0366/ijbsv07p0567g05.jpg

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