↓ Skip to main content

Aflatoxin B1 inhibits the type 1 interferon response pathway via STAT1 suggesting another mechanism of hepatocellular carcinoma

Overview of attention for article published in Infectious Agents and Cancer, March 2017
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age and source

Mentioned by

twitter
1 X user

Citations

dimensions_citation
13 Dimensions

Readers on

mendeley
31 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Aflatoxin B1 inhibits the type 1 interferon response pathway via STAT1 suggesting another mechanism of hepatocellular carcinoma
Published in
Infectious Agents and Cancer, March 2017
DOI 10.1186/s13027-017-0127-8
Pubmed ID
Authors

Patrick W. Narkwa, David J. Blackbourn, Mohamed Mutocheluh

Abstract

Aflatoxin B1 (AFB1) contamination of food is very high in most sub-Saharan African countries. AFB1 is known to cause hepatocellular carcinoma (HCC) by inducing mutation in the tumour suppressor gene TP53. The number of new HCC cases is high in West Africa with an accompanying high mortality. The type I interferon (IFN) pathway of the innate immune system limits viral infections and exerts its anti-cancer property by up-regulating tumour suppressor activities and pro-apoptotic pathways. Indeed, IFN-α is reported to show significant protective effects against hepatic fibrogenesis and carcinogenesis. However, the mechanism behind AFB1 deregulation of the type I interferon (IFN) signalling pathway, with consequent HCC is largely unknown. This current study seeks to test the hypothesis that AFB1 inhibits the type I IFN response by directly interfering with key signalling proteins and thus increase the risk of HCC in humans. We evaluated the effects of AFB1 on the type I IFN signalling pathway using IFN stimulated response element (ISRE)-based luciferase reporter gene assay. In addition, the effects of AFB1 on the transcript levels of JAK1, STAT1 and OAS3 were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) and confirmed by immunoblot assay. Our results indicated that AFB1 inhibited the type I IFN signalling pathway in human hepatoma cell line HepG2 cells by suppressing the transcript levels of JAK1, STAT1 and OAS3. AFB1 also decreased the accumulation of STAT1 protein. The inhibition of the type I IFN anti-cancer response pathway by AFB1 suggest a novel mechanism by which AFB1 may induce hepatocellular carcinoma in humans.

X Demographics

X Demographics

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

Mendeley readers

The data shown below were compiled from readership statistics for 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 31 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 23%
Researcher 4 13%
Student > Master 4 13%
Professor > Associate Professor 2 6%
Student > Doctoral Student 1 3%
Other 5 16%
Unknown 8 26%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 16%
Pharmacology, Toxicology and Pharmaceutical Science 4 13%
Agricultural and Biological Sciences 4 13%
Medicine and Dentistry 4 13%
Engineering 2 6%
Other 4 13%
Unknown 8 26%
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 04 April 2017.
All research outputs
#15,452,475
of 22,962,258 outputs
Outputs from Infectious Agents and Cancer
#254
of 521 outputs
Outputs of similar age
#194,823
of 309,707 outputs
Outputs of similar age from Infectious Agents and Cancer
#7
of 10 outputs
Altmetric has tracked 22,962,258 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 521 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.4. This one is in the 42nd percentile – i.e., 42% 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 309,707 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 10 others from the same source and published within six weeks on either side of this one. This one has scored higher than 3 of them.