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利用靶向醛酮还原酶家族 1 成员 B10 的小干扰 RNA 抑制肺癌的增殖和迁移。

Inhibiting proliferation and migration of lung cancer using small interfering RNA targeting on Aldo-keto reductase family 1 member B10.

机构信息

Department of Lung Tumor Clinical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.

出版信息

Mol Med Rep. 2018 Feb;17(2):2153-2160. doi: 10.3892/mmr.2017.8173. Epub 2017 Nov 28.

DOI:10.3892/mmr.2017.8173
PMID:29207124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5783456/
Abstract

Lung cancer is the leading cause of global cancer‑associated mortality. Genomic alterations in lung cancers have not been widely characterized, however, the molecular mechanism of tumor initiation and progression remain unknown, and no molecularly targeted have been specifically developed for its treatment and diagnosis. The present study observed the upregulation of Aldo‑keto reductase family 1 member Bio10 (AKR1B10) lung cancer tissues by analyzing two public lung cancer gene expression datasets. Further experiments in silencing AKR1B10 demonstrated that the expression of AKR1B10 was associated with cell proliferation, cell cycle, adhesion and invasion, as well as extracellular‑signal‑regulated kinase/mitogen activated protein kinase signal pathway. The overexpression of AKR1B10 in lung cancer indicates the important role of AKR1B10 in tumorigenesis. These findings suggest that AKR1B10 could be a potential diagnosis and treatment mark of lung cancer.

摘要

肺癌是全球癌症相关死亡的主要原因。然而，肺癌中的基因组改变尚未得到广泛描述，肿瘤发生和进展的分子机制仍不清楚，也没有专门针对其治疗和诊断的分子靶向药物。本研究通过分析两个公共肺癌基因表达数据集，观察到 Aldo-keto reductase family 1 member Bio10 (AKR1B10) 在肺癌组织中的上调。进一步的沉默 AKR1B10 的实验表明，AKR1B10 的表达与细胞增殖、细胞周期、黏附和侵袭以及细胞外信号调节激酶/有丝分裂原激活蛋白激酶信号通路有关。AKR1B10 在肺癌中的过表达表明 AKR1B10 在肿瘤发生中起着重要作用。这些发现表明 AKR1B10 可能是肺癌的潜在诊断和治疗标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/117e2a192278/MMR-17-02-2153-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/80c69b7d9d4c/MMR-17-02-2153-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/26f3e97304c2/MMR-17-02-2153-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/fff14c34a104/MMR-17-02-2153-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/df9eea160d08/MMR-17-02-2153-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/6f737df8c8d2/MMR-17-02-2153-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/daa765ed6dd8/MMR-17-02-2153-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/7f7318b02858/MMR-17-02-2153-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/3f40883e8f5f/MMR-17-02-2153-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/adca7ff7b000/MMR-17-02-2153-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/6e0206221c60/MMR-17-02-2153-g09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/1e166eb38ed4/MMR-17-02-2153-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/117e2a192278/MMR-17-02-2153-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/80c69b7d9d4c/MMR-17-02-2153-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/26f3e97304c2/MMR-17-02-2153-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/fff14c34a104/MMR-17-02-2153-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/df9eea160d08/MMR-17-02-2153-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/6f737df8c8d2/MMR-17-02-2153-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/daa765ed6dd8/MMR-17-02-2153-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/7f7318b02858/MMR-17-02-2153-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/3f40883e8f5f/MMR-17-02-2153-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/adca7ff7b000/MMR-17-02-2153-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/6e0206221c60/MMR-17-02-2153-g09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/1e166eb38ed4/MMR-17-02-2153-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7566/5783456/117e2a192278/MMR-17-02-2153-g11.jpg

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