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Granulin epithelin precursor promotes colorectal carcinogenesis by activating MARK/ERK pathway

Overview of attention for article published in Journal of Translational Medicine, June 2018
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Title
Granulin epithelin precursor promotes colorectal carcinogenesis by activating MARK/ERK pathway
Published in
Journal of Translational Medicine, June 2018
DOI 10.1186/s12967-018-1530-7
Pubmed ID
Authors

Yi Pan, Siu Tim Cheung, Joanna Hung Man Tong, Ka Yee Tin, Wei Kang, Raymond Wai Ming Lung, Feng Wu, Hui Li, Simon Siu Man Ng, Tony Wing Chung Mak, Ka Fai To, Anthony Wing Hung Chan

Abstract

Granulin epithelin precursor (GEP) is reported to function as a growth factor stimulating proliferation and migration, and conferring chemoresistance in many cancer types. However, the expression and functional roles of GEP in colorectal cancer (CRC) remain elusive. The aim of this study was thus to investigate the clinical significance of GEP in CRC and reveal the molecular mechanism of GEP in CRC initiation and progression. The mRNA expression of GEP in CRC cell lines were detected by qRT-PCR. The GEP protein expression was validated by immunohistochemistry in tissue microarray (TMA) including 190 CRC patient samples. The clinicopathological correlation analysis were achieved by GEP expression on TMA. Functional roles of GEP were determined by MTT proliferation, monolayer colony formation, cell invasion and migration and in vivo studies through siRNA/shRNA mediated knockdown assays. The cancer signaling pathway identification was acquired by flow cytometry, western blot and luciferase activity assays. The mRNA expression of GEP in CRC was significantly higher than it in normal colon tissues. GEP protein was predominantly localized in the cytoplasm and most of the CRC cases demonstrated abundant GEP protein compared with non-tumorous tissues. GEP overexpression was associated with non-rectal location, advanced AJCC stage, regional lymph node and distant metastasis. By Kaplan-Meier survival analysis, GEP abundance served as a prognostic marker for worse survival in CRC patients. GEP knockdown exhibited anti-cancer effect such as inhibiting cell proliferation, monolayer colony formation, cell invasion and migration in DLD-1 and HCT 116 cells and decelerating xenograft formation in nude mice. siGEP also induced G1 cell cycle arrest and apoptosis. Luciferase activity assays further demonstrated GEP activation was involved in MAPK/ERK signaling pathway. In summary, we compressively delineate the oncogenic role of GEP in colorectal tumorigenesis by activating MAPK/ERK signaling pathway. GEP might serve as a useful prognostic biomarker and therapeutic target for CRC.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 18%
Student > Master 3 18%
Student > Doctoral Student 2 12%
Professor 1 6%
Librarian 1 6%
Other 2 12%
Unknown 5 29%
Readers by discipline Count As %
Medicine and Dentistry 6 35%
Business, Management and Accounting 1 6%
Immunology and Microbiology 1 6%
Computer Science 1 6%
Social Sciences 1 6%
Other 1 6%
Unknown 6 35%
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 06 June 2018.
All research outputs
#20,520,426
of 23,088,369 outputs
Outputs from Journal of Translational Medicine
#3,357
of 4,051 outputs
Outputs of similar age
#289,413
of 329,877 outputs
Outputs of similar age from Journal of Translational Medicine
#53
of 92 outputs
Altmetric has tracked 23,088,369 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 4,051 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.6. 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 329,877 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 92 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.