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Chlorella sorokiniana induces mitochondrial-mediated apoptosis in human non-small cell lung cancer cells and inhibits xenograft tumor growth in vivo

Overview of attention for article published in BMC Complementary Medicine and Therapies, February 2017
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1 Redditor

Citations

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53 Dimensions

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74 Mendeley
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Title
Chlorella sorokiniana induces mitochondrial-mediated apoptosis in human non-small cell lung cancer cells and inhibits xenograft tumor growth in vivo
Published in
BMC Complementary Medicine and Therapies, February 2017
DOI 10.1186/s12906-017-1611-9
Pubmed ID
Authors

Ping-Yi Lin, Ching-Tsan Tsai, Wan-Ling Chuang, Ya-Hsuan Chao, I-Horng Pan, Yu-Kuo Chen, Chi-Chen Lin, Bing-Yen Wang

Abstract

Lung cancer is one of the leading causes of cancer related deaths worldwide. Marine microalgae are a source of biologically active compounds and are widely consumed as a nutritional supplement in East Asian countries. It has been reported that Chlorella or Chlorella extracts have various beneficial pharmacological compounds that modulate immune responses; however, no studies have investigated the anti-cancer effects of Chlorella sorokiniana (CS) on non-small cell lung cancer (NSCLC). In this study, we evaluated the anti-cancer effects of CS in two human NSCLC cell lines (A549 and CL1-5 human lung adenocarcinoma cells), and its effects on tumor growth in a subcutaneous xenograft tumor model. We also investigated the possible molecular mechanisms governing the pharmacological function of CS. Our results showed that exposure of the two cell lines to CS resulted in a concentration-dependent reduction in cell viability. In addition, the percentage of apoptotic cells increased in a dose-dependent manner, suggesting that CS might induce apoptosis in human NSCLC cells. Western blot analysis revealed that exposure to CS resulted in increased protein expression of the cleaved/activated forms of caspase-3, caspase-9, and PARP, except caspase-8. ZDEVD (caspase-3 inhibitor) and Z-LEHD (caspase-9 inhibitor) were sufficient at preventing apoptosis in both A549 and CL1-5 cells, proving that CS induced cell death via the mitochondria-mediated apoptotic pathway. Exposure of A549 and CL1-5 cells to CS for 24 h resulted in decreased expression of Bcl-2 protein and increased expression of Bax protein as well as decreased expression of two IAP family proteins, survivin and XIAP. We demonstrated that CS induces mitochondrial-mediated apoptosis in NSCLC cells via downregulation of Bcl-2, XIAP and survivin. In addition, we also found that the tumors growth of subcutaneous xenograft in vivo was markedly inhibited after oral intake of CS.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 74 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
India 1 1%
Unknown 73 99%

Demographic breakdown

Readers by professional status Count As %
Student > Master 11 15%
Student > Ph. D. Student 9 12%
Researcher 7 9%
Student > Bachelor 6 8%
Other 4 5%
Other 12 16%
Unknown 25 34%
Readers by discipline Count As %
Agricultural and Biological Sciences 14 19%
Biochemistry, Genetics and Molecular Biology 12 16%
Medicine and Dentistry 5 7%
Immunology and Microbiology 3 4%
Nursing and Health Professions 2 3%
Other 11 15%
Unknown 27 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 24 September 2018.
All research outputs
#14,918,889
of 22,952,268 outputs
Outputs from BMC Complementary Medicine and Therapies
#1,847
of 3,639 outputs
Outputs of similar age
#242,840
of 420,356 outputs
Outputs of similar age from BMC Complementary Medicine and Therapies
#48
of 85 outputs
Altmetric has tracked 22,952,268 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,639 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.5. This one is in the 43rd percentile – i.e., 43% 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 420,356 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 39th percentile – i.e., 39% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 85 others from the same source and published within six weeks on either side of this one. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.