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miR-182 suppresses invadopodia formation and metastasis in non-small cell lung cancer by targeting cortactin gene

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, July 2018
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Title
miR-182 suppresses invadopodia formation and metastasis in non-small cell lung cancer by targeting cortactin gene
Published in
Journal of Experimental & Clinical Cancer Research, July 2018
DOI 10.1186/s13046-018-0824-1
Pubmed ID
Authors

Yongwen Li, Hongbing Zhang, Hao Gong, Yin Yuan, Ying Li, Cong Wang, Weiting Li, Zihe Zhang, Minghui Liu, Hongyu Liu, Jun Chen

Abstract

Metastasis is the leading cause of cancer mortality and is a major hurdle for lung cancer treatment. Invadopodia, which are cancer-specific protrusive structures, play a crucial role in the metastatic cascade through degradation of the basement membrane and surrounding stroma. Cortactin, a critical component of invadopodia, frequently used as an invadopodia marker, a universally important player in invadopodia function, and is frequently overexpressed in cancer, but the exact mechanism of regulation is not yet fully understood. The expression level of CTTN in human non-small cell lung cancer (NSCLC) tissues was detected by qRT-PCR. Cell migration, invasion and invadopodia formation were assessed in vitro by wound-healing, transwell assay and immunofluorescence, respectively. The dual-luciferase reporter assay was used to identify the direct target of miR-182. Hepatocyte growth factor (HGF) and phorbol 12,13-dibutyrate (PDBu) can induce CTTN expression, motility, and invasion ability, as well as invadopodia formation in non-small cell lung cancer (NSCLC). Moreover, miR-182 suppressed metastasis and invadopodia formation by targeting CTTN in NSCLC. Our qRT-PCR results showed that CTTN expression was inversely correlated with miR-182 expression that suppressed invadopodia formation via suppression of the Cdc42/N-WASP pathway. Furthermore, miR-182 negatively regulated invadopodia function, and suppressed extracellular matrix(ECM) degradation in lung cancer cells by inhibiting cortactin. Collectively, our results demonstrated that miR-182 targeted CTTN gene in NSCLC and suppressed lung cancer invadopodia formation, and thus suppressed lung cancer metastasis. This suggests a therapeutic application of miR-182 in NSCLC.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 25 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 7 28%
Student > Ph. D. Student 4 16%
Student > Postgraduate 2 8%
Researcher 2 8%
Student > Doctoral Student 1 4%
Other 4 16%
Unknown 5 20%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 28%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Agricultural and Biological Sciences 2 8%
Medicine and Dentistry 2 8%
Immunology and Microbiology 1 4%
Other 3 12%
Unknown 8 32%
Attention Score in Context

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 15 July 2018.
All research outputs
#22,767,715
of 25,385,509 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,970
of 2,382 outputs
Outputs of similar age
#297,902
of 339,673 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#51
of 65 outputs
Altmetric has tracked 25,385,509 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,382 research outputs from this source. They receive a mean Attention Score of 4.8. This one is in the 1st percentile – i.e., 1% 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 339,673 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 65 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.