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Role of MCP‐1 in alcohol‐induced aggressiveness of colorectal cancer cells

Overview of attention for article published in Molecular Carcinogenesis, May 2015
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  • Good Attention Score compared to outputs of the same age (65th percentile)
  • Good Attention Score compared to outputs of the same age and source (76th percentile)

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Article details
Title
Role of MCP‐1 in alcohol‐induced aggressiveness of colorectal cancer cells
Published in
Molecular Carcinogenesis, May 2015
DOI 10.1002/mc.22343
Pubmed ID
Authors
Abstract

Epidemiological studies demonstrate that alcohol consumption is associated with an increased risk of colorectal cancer (CRC). In addition to promoting carcinogenesis, alcohol may also accelerate the progression of existing CRC. We hypothesized that alcohol may enhance the aggressiveness of CRC. In this study, we investigated the effect of alcohol on the migration/invasion and metastasis of CRC. Alcohol increased the migration/invasion of colorectal cancer cells (DLD1, HCT116, HT29, and SW480) in a concentration-dependent manner. Among these colon cancer cell lines, HCT116 cells were most responsive while HT29 cells were the least responsive to ethanol-stimulated cell migration/invasion. These in vitro results were supported by animal studies which demonstrated that ethanol enhanced the metastasis of colorectal cancer cells to the liver and lung. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that plays an important role in regulating tumor microenvironment and metastasis. Alcohol increased the expression of MCP-1 and its receptor CCR2 at both protein and mRNA levels. The pattern of alcohol-induced alterations in MCP-1 expression was consistent with its effect on migration/invasion; HCT116 cells displayed the highest up-regulation of MCP-1/CCR2 in response to alcohol exposure. An antagonist of CCR2 blocked alcohol-stimulated migration. Alcohol caused an initial cytosolic accumulation of β-catenin and its subsequent nuclear translocation by inhibiting GSK3β activity. Alcohol stimulated the activity of MCP-1 gene promoter in a β-catenin-dependent manner. Furthermore, knock-down of MCP-1/CCR2 or β-catenin was sufficient to inhibit alcohol-induced cell migration/invasion. Together, these results suggested that alcohol may promote the metastasis of CRC through modulating GSK3β/β-catenin/MCP-1 pathway. © 2015 Wiley Periodicals, Inc.

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X Demographics

X Demographics

The data shown below were collected from the profiles of 5 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley demographics

Mendeley demographics

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.
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Geographical breakdown

Geographical breakdown
Country Count As %
Unknown 26 100%

Demographic breakdown

Readers by professional status
Readers by professional status Count As %
Student > Master 4 15%
Student > Bachelor 3 12%
Student > Doctoral Student 2 8%
Lecturer > Senior Lecturer 1 4%
Other 1 4%
Other 2 8%
Unknown 13 50%
Readers by discipline
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 15%
Medicine and Dentistry 4 15%
Nursing and Health Professions 2 8%
Agricultural and Biological Sciences 1 4%
Psychology 1 4%
Other 0 0%
Unknown 14 54%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. 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 01 June 2015.
All research outputs
#8,800,998
of 26,184,649 outputs
Outputs from Molecular Carcinogenesis
#337
of 1,489 outputs
Outputs of similar age
#97,663
of 282,491 outputs
Outputs of similar age from Molecular Carcinogenesis
#6
of 25 outputs
Altmetric has tracked 26,184,649 research outputs across all sources so far. This one has received more attention than most of these and is in the 66th percentile.
So far Altmetric has tracked 1,489 research outputs from this source. They receive a mean Attention Score of 3.8. This one has done well, scoring higher than 77% of its peers.
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 282,491 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 65% of its contemporaries.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 76% of its contemporaries.