| Title |
ZNF259 inhibits non-small cell lung cancer cells proliferation and invasion by FAK-AKT signaling
|
|---|---|
| Published in |
Cancer Management and Research, December 2017
|
| DOI | 10.2147/cmar.s150614 |
| Pubmed ID | |
| Authors |
Yuemei Shan, Wei Cao, Tao Wang, Guiyang Jiang, Yong Zhang, Xianghong Yang |
| Abstract |
Zinc finger protein 259 (ZNF259) is known to play essential roles in embryonic development and cell cycle regulation. However, its expression pattern and clinicopathological relevance remain unclear. A total of 114 lung cancer specimens were collected. The ZNF259 expression was measured between the lung cancer tissues and the adjacent normal lung tissues by immunohistochemical staining and Western blotting. Moreover, the correlation of ZNF259 expression with clinicopathological features was analyzed in 114 cases of lung cancer. Additionally, ZNF259 was depleted in the lung cancer cells in order to analyze its effect in the lung cancer. Immunohistochemical staining of 114 lung cancer specimens revealed significantly lower ZNF259 expression in lung cancer tissues than in adjacent normal lung tissues (53.5% vs 71.4%, P<0.001). In addition, ZNF259 downregulation was significantly associated with larger tumor size (P=0.001), advanced TNM stage (P=0.002), and positive lymph node metastasis (P=0.02). Western blotting of 20 paired lung cancer samples revealed lower ZNF259 protein levels in lung cancer tissues than in those of corresponding normal lung tissues (P=0.0032). Depletion of ZNF259 resulted in enhanced levels of p-FAK and p-AKT, CyclinD1, and MMP2, which in turn increased the proliferation and invasion of lung cancer cells. The effects of ZNF259 depletion were reversed by treatment with specific FAK or AKT inhibitors. ZNF259 depletion is correlated with the development of non-small cell lung cancer (NSCLC) and serves as a predictor of adverse clinical outcome in NSCLC patients. The inhibitory effect of ZNF259 on proliferation and invasion can be attributed to downregulation of CyclinD1 and MMP2 via inactivation of the FAK-AKT pathway. |
Mendeley readers
The data shown below were compiled from readership statistics for 8 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 8 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 3 | 38% |
| Professor > Associate Professor | 1 | 13% |
| Student > Bachelor | 1 | 13% |
| Researcher | 1 | 13% |
| Unknown | 2 | 25% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 2 | 25% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 13% |
| Biochemistry, Genetics and Molecular Biology | 1 | 13% |
| Medicine and Dentistry | 1 | 13% |
| Unknown | 3 | 38% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. 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 14 December 2017.
All research outputs
#20,454,971
of 23,011,300 outputs
Outputs from Cancer Management and Research
#1,404
of 2,017 outputs
Outputs of similar age
#373,061
of 437,944 outputs
Outputs of similar age from Cancer Management and Research
#37
of 42 outputs
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