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Downregulation of NMI promotes tumor growth and predicts poor prognosis in human lung adenocarcinomas

Overview of attention for article published in Molecular Cancer, October 2017
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  • High Attention Score compared to outputs of the same age and source (80th percentile)

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Title
Downregulation of NMI promotes tumor growth and predicts poor prognosis in human lung adenocarcinomas
Published in
Molecular Cancer, October 2017
DOI 10.1186/s12943-017-0705-9
Pubmed ID
Authors

Jingshu Wang, Kun Zou, Xu Feng, Miao Chen, Cong Li, Ranran Tang, Yang Xuan, Meihua Luo, Wangbing Chen, Huijuan Qiu, Ge Qin, Yixin Li, Changlin Zhang, Binyi Xiao, Lan Kang, Tiebang Kang, Wenlin Huang, Xinfa Yu, Xiaojun Wu, Wuguo Deng

Abstract

N-myc (and STAT) interactor (NMI) plays vital roles in tumor growth, progression, and metastasis. In this study, we identified NMI as a potential tumor suppressor in lung cancer and explored its molecular mechanism involved in lung cancer progression. Human lung cancer cell lines and a mouse xenograft model was used to study the effect of NMI on tumor growth. The expression of NMI, COX-2 and relevant signaling proteins were examined by Western blot. Tissue microarray immunohistochemical analysis was performed to assess the correlation between NMI and COX-2 expression in lung cancer patients. NMI was highly expressed in normal lung cells and tissues, but lowly expressed in lung cancer cells and tissues. Overexpression of NMI induced apoptosis, suppressed lung cancer cell growth and migration, which were mediated by up-regulation of the cleaved caspase-3/9 and down-regulation of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin, and COX-2/PGE2. In contrast, knockdown of NMI promoted lung cancer cell colony formation and migration, which were correlated with the increased expression of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin and COX-2/PGE2. Further study showed that NMI suppressed COX-2 expression through inhibition of the p50/p65 NF-κB acetylation mediated by p300. The xenograft lung cancer mouse models also confirmed the NMI-mediated suppression of tumor growth by inhibiting COX-2 signaling. Moreover, tissue microarray immunohistochemical analysis of lung adenocarcinomas also demonstrated a negative correlation between NMI and COX-2 expression. Kaplan-Meier analysis indicated that the patients with high level of NMI had a significantly better prognosis. Our study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-κB acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 18%
Student > Ph. D. Student 1 6%
Student > Postgraduate 1 6%
Student > Master 1 6%
Unknown 11 65%
Readers by discipline Count As %
Medicine and Dentistry 2 12%
Biochemistry, Genetics and Molecular Biology 2 12%
Pharmacology, Toxicology and Pharmaceutical Science 1 6%
Unknown 12 71%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 5. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 December 2023.
All research outputs
#6,933,681
of 25,093,754 outputs
Outputs from Molecular Cancer
#542
of 1,890 outputs
Outputs of similar age
#103,867
of 330,575 outputs
Outputs of similar age from Molecular Cancer
#6
of 25 outputs
Altmetric has tracked 25,093,754 research outputs across all sources so far. This one has received more attention than most of these and is in the 72nd percentile.
So far Altmetric has tracked 1,890 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.7. This one has gotten more attention than average, scoring higher than 70% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 330,575 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 68% of its contemporaries.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 80% of its contemporaries.