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ZAR1 is a novel epigenetically inactivated tumour suppressor in lung cancer

Overview of attention for article published in Clinical Epigenetics, June 2017
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Title
ZAR1 is a novel epigenetically inactivated tumour suppressor in lung cancer
Published in
Clinical Epigenetics, June 2017
DOI 10.1186/s13148-017-0360-4
Pubmed ID
Authors

Antje M. Richter, Steffen Kiehl, Nicole Köger, Janina Breuer, Thorsten Stiewe, Reinhard H. Dammann

Abstract

Lung cancer is the leading cause of cancer-related deaths with 1.8 million new cases each year and poor 5-year prognosis. Promoter hypermethylation of tumour suppressors leads to their inactivation and thereby can promote cancer development and progression. In this study, we analysed ZAR1 (zygote arrest 1), which has been said to be a maternal-effect gene and its expression mostly limited to certain reproductive tissues. Our study shows that ZAR1 is expressed in normal lung but inactivated by promoter methylation in lung cancer. ZAR1 is hypermethylated in primary lung cancer samples (22% small cell lung carcinoma (SCLC) and 76% non-small cell lung carcinoma (NSCLC), p < 0.001) vs. normal control lung tissue (11%). In lung cancer cell lines, ZAR1 was significantly methylated in 75% of SCLC and 83% of NSCLC vs. normal tissue (p < 0.005/0.05). In matching tumours and control tissues, we observed that NSCLC primary tumour samples exhibited a tumour-specific promoter methylation of ZAR1 in comparison to the normal control lung tissue. Demethylation treatment of various lung cancer cell lines reversed ZAR1 promoter hypermethylation and subsequently re-established ZAR1 expression. In addition, we could show the growth inhibitory potential of ZAR1 in lung cancer cell lines and cancer cell lines. Exogenous expression of ZAR1 not only inhibited colony formation but also blocked cell cycle progression of cancer cell lines. Our study shows for the first time the lung tumour-specific epigenetic inactivation of ZAR1 due to DNA methylation of its CpG island promoter. Furthermore, ZAR1 was characterised by the ability to block tumour growth through the inhibition of cell cycle progression in cancer cell lines. We propose that ZAR1 could serve as an epigenetically inactivated biomarker in lung cancer.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 12 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 5 42%
Researcher 3 25%
Professor 1 8%
Unknown 3 25%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 25%
Medicine and Dentistry 2 17%
Nursing and Health Professions 1 8%
Pharmacology, Toxicology and Pharmaceutical Science 1 8%
Economics, Econometrics and Finance 1 8%
Other 1 8%
Unknown 3 25%
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 20 April 2018.
All research outputs
#17,897,310
of 22,977,819 outputs
Outputs from Clinical Epigenetics
#947
of 1,262 outputs
Outputs of similar age
#227,068
of 317,446 outputs
Outputs of similar age from Clinical Epigenetics
#19
of 30 outputs
Altmetric has tracked 22,977,819 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,262 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.5. This one is in the 20th percentile – i.e., 20% 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 317,446 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 30 others from the same source and published within six weeks on either side of this one. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.