↓ Skip to main content

CD317 Promotes the survival of cancer cells through apoptosis-inducing factor

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, July 2016
Altmetric Badge

About this Attention Score

  • Good Attention Score compared to outputs of the same age (71st percentile)

Mentioned by

4 tweeters
1 patent


6 Dimensions

Readers on

22 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.
CD317 Promotes the survival of cancer cells through apoptosis-inducing factor
Published in
Journal of Experimental & Clinical Cancer Research, July 2016
DOI 10.1186/s13046-016-0391-2
Pubmed ID

Xin Li, Guizhong Zhang, Qian Chen, Yingxue Lin, Junxin Li, Qingguo Ruan, Youhai Chen, Guang Yu, Xiaochun Wan


Low nutrient environment is a major obstacle to solid tumor growth. However, many tumors have developed adaptive mechanisms to circumvent the requirement for exogenous growth factors. Here we used siRNA interference or plasmid transfection techniques to knockdown or enhance CD317 expression respectively, in mammalian cancer cells, and subjected these CD317-manipulated cells to serum deprivation to study the role of CD317 on stress-induced apoptosis and the underlying mechanism. We report that CD317, an innate immune gene overexpressed in human cancers, protected cancer cells against serum deprivation-induced apoptosis. In tumor cells, loss of CD317 markedly enhanced their susceptibility to serum deprivation-induced apoptosis with no effect on autophagy or caspase activation, indicating an autophagy- and caspase-independent mechanism of CD317 function. Importantly, CD317 knockdown in serum-deprived tumor cells impaired mitochondria function and subsequently promoted apoptosis-inducing factor (AIF) release and nuclear translocation but had little effect on mitochondrial and cytoplasmic distributions of cytochrome C, a pro-apoptotic factor released from mitochondria that initiates caspase processing in response to death stimuli. Furthermore, overexpression of CD317 in HEK293T cells inhibits serum deprivation-induced apoptosis as well as the release and nuclear accumulation of AIF. Our data suggest that CD317 functions as an anti-apoptotic factor through the mitochondria-AIF axis in malnourished condition and may serve as a potential drug target for cancer therapy.

Twitter Demographics

The data shown below were collected from the profiles of 4 tweeters 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 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 22 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 5 23%
Student > Ph. D. Student 4 18%
Student > Bachelor 3 14%
Professor 2 9%
Student > Doctoral Student 1 5%
Other 1 5%
Unknown 6 27%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 8 36%
Medicine and Dentistry 4 18%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Immunology and Microbiology 1 5%
Agricultural and Biological Sciences 1 5%
Other 0 0%
Unknown 7 32%

Attention Score in Context

This research output has an Altmetric Attention Score of 5. 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 02 December 2021.
All research outputs
of 21,326,488 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
of 1,877 outputs
Outputs of similar age
of 280,245 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
of 1 outputs
Altmetric has tracked 21,326,488 research outputs across all sources so far. This one has received more attention than most of these and is in the 73rd percentile.
So far Altmetric has tracked 1,877 research outputs from this source. They receive a mean Attention Score of 3.5. This one has done well, scoring higher than 87% 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 280,245 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 71% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them