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MICAL1 controls cell invasive phenotype via regulating oxidative stress in breast cancer cells

Overview of attention for article published in BMC Cancer, July 2016
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1 tweeter

Citations

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27 Dimensions

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20 Mendeley
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Title
MICAL1 controls cell invasive phenotype via regulating oxidative stress in breast cancer cells
Published in
BMC Cancer, July 2016
DOI 10.1186/s12885-016-2553-1
Pubmed ID
Authors

Wenjie Deng, Yueyuan Wang, Luo Gu, Biao Duan, Jie Cui, Yujie Zhang, Yan Chen, Shixiu Sun, Jing Dong, Jun Du

Abstract

Molecules Interacting with CasL (MICAL1), a multidomain flavoprotein monoxygenase, is strongly involved in the mechanisms that promote cancer cell proliferation and survival. Activation of MICAL1 causes an up-regulation of reactive oxygen species (ROS) in HeLa cells. ROS can function as a signaling molecule that modulates protein phosphorylation, leading to malignant phenotypes of cancer cells such as invasion and metastasis. Herein, we tested whether MICAL1 could control cell migration and invasion through regulating ROS in breast cancer cell lines. The effects of depletion/overexperssion of MICAL1 on cell invasion rate were measured by matrigel-based transwell assays. The contents of ROS in breast cancer cells were evaluated by CM2-DCFHDA staining and enhanced lucigenin chemiluminescence method. RAB35 activity was assessed by pulldown assay. The relationship of RAB35 and MICAL1 was evaluated by immunofluorescence, coimmunoprecipitation, immunoblotting and co-transfection techniques. Immunoblotting assays were also used to analyze Akt phosphorylation level. In this study, we found that depletion of MICAL1 reduced cell migration and invasion as well as ROS generation. Phosphorylation of Akt was also attenuated by MICAL1 depletion. Likewise, the over-expression of MICAL1 augmented the generation of ROS, increased Akt phosphorylation, and favored invasive phenotype of breast cancer cells. Moreover, we investigated the effect of EGF signaling on MICAL1 function. We demonstrated that EGF increased RAB35 activation and activated form of RAB35 could bind to MICAL1. Silencing of RAB35 repressed ROS generation, prevented Akt phosphorylation and inhibited cell invasion in response to EGF. Taken together, our results provide evidence that MICAL1 plays an essential role in the activation of ROS/Akt signaling and cell invasive phenotype and identify a novel link between RAB35 and MICAL1 in regulating breast cancer cell invasion. These findings may provide a basis for designing future therapeutic strategy for blocking breast cancer metastasis.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 25%
Student > Ph. D. Student 4 20%
Student > Bachelor 2 10%
Professor 1 5%
Student > Doctoral Student 1 5%
Other 1 5%
Unknown 6 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 10 50%
Agricultural and Biological Sciences 2 10%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Immunology and Microbiology 1 5%
Medicine and Dentistry 1 5%
Other 0 0%
Unknown 5 25%

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 21 July 2016.
All research outputs
#4,277,807
of 8,088,508 outputs
Outputs from BMC Cancer
#1,541
of 3,452 outputs
Outputs of similar age
#141,830
of 258,114 outputs
Outputs of similar age from BMC Cancer
#92
of 243 outputs
Altmetric has tracked 8,088,508 research outputs across all sources so far. This one is in the 27th percentile – i.e., 27% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,452 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 43rd percentile – i.e., 43% 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 258,114 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 35th percentile – i.e., 35% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 243 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.