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NLK functions to maintain proliferation and stemness of NSCLC and is a target of metformin

Overview of attention for article published in Journal of Hematology & Oncology, October 2015
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Title
NLK functions to maintain proliferation and stemness of NSCLC and is a target of metformin
Published in
Journal of Hematology & Oncology, October 2015
DOI 10.1186/s13045-015-0203-8
Pubmed ID
Authors

Dong Suwei, Zeng Liang, Liu Zhimin, Li Ruilei, Zou Yingying, Li Zhen, Ge Chunlei, Lai Zhangchao, Xue Yuanbo, Yang Jinyan, Li Gaofeng, Song Xin

Abstract

Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine kinase that regulates the activity of a wide range of signal transduction pathways. Metformin, an oral antidiabetic drug, is used for cancer prevention. However, the significance and underlying mechanism of NLK and metformin in oncogenesis has not been fully elucidated. Here, we investigate a novel role of NLK and metformin in human non-small cell lung cancer (NSCLC). NLK expression was analyzed in 121 NSCLCs and 92 normal lung tissue samples from benign pulmonary disease. Lentivirus vectors with NLK-shRNA were used to examine the effect of NLK on cell proliferation and tumorigenesis in vitro. Then, tumor xenograft mouse models revealed that NLK knockdown cells had a reduced ability for tumor formation compared with the control group in vivo. Multiple cell cycle regulator expression patterns induced by NLK silencing were examined by western blots in A549 cells. We also employed metformin to study its anti-cancer effects and mechanisms. Cancer stem cell property was checked by tumor sphere formation and markers including CD133, Nanog, c-Myc, and TLF4. Immunohistochemical (IHC) analysis revealed that NLK expression was up-regulated in NSCLC cases (p < 0.001) and correlated with tumor T stage (p < 0.05). Silencing of NLK suppressed cell proliferation and tumorigenicity significantly in vitro and in vivo, which might be modulated by JUN family proteins. Furthermore, metformin selectively inhibits NLK expression and proliferation in NSCLC cells, but not immortalized noncancerous lung bronchial epithelial cells. In addition, both NLK knockdown and metformin treatment reduced the tumor sphere formation capacity and percentage of CD133+ cells. Accordingly, the expression level of stem cell markers (Nanog, c-Myc, and TLF4) were decreased significantly. NLK is critical for cancer cell cycle progression, and tumorigenesis in NSCLC, NLK knockdown, and metformin treatment inhibit cancer cell proliferation and stemness. Metformin inhibits NLK expression and might be a potential treatment strategy for NSCLC.

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The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 34 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 34 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 21%
Researcher 6 18%
Student > Postgraduate 4 12%
Student > Bachelor 4 12%
Other 2 6%
Other 5 15%
Unknown 6 18%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 26%
Medicine and Dentistry 9 26%
Pharmacology, Toxicology and Pharmaceutical Science 4 12%
Agricultural and Biological Sciences 3 9%
Computer Science 1 3%
Other 3 9%
Unknown 5 15%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 03 November 2015.
All research outputs
#14,827,682
of 22,831,537 outputs
Outputs from Journal of Hematology & Oncology
#723
of 1,192 outputs
Outputs of similar age
#157,339
of 284,370 outputs
Outputs of similar age from Journal of Hematology & Oncology
#12
of 21 outputs
Altmetric has tracked 22,831,537 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,192 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.7. This one is in the 35th percentile – i.e., 35% of its peers scored the same or lower than it.
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 284,370 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 21 others from the same source and published within six weeks on either side of this one. This one is in the 33rd percentile – i.e., 33% of its contemporaries scored the same or lower than it.