Mitochondrial deficiency impairs hypoxic induction of HIF-1 transcriptional activity and retards tumor growth
Oncotarget, ISSN: 1949-2553, Vol: 8, Issue: 7, Page: 11841-11854
2017
- 10Citations
- 29Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations10
- Citation Indexes10
- 10
- CrossRef8
- Captures29
- Readers29
- 29
Article Description
Mitochondria can be involved in regulating cellular stress response to hypoxia and tumor growth, but little is known about that mechanistic relationship. Here, we show that mitochondrial deficiency severely retards tumor xenograft growth with impairing hypoxic induction of HIF-1 transcriptional activity. Using mtDNA-deficient ρ cells, we found that HIF-1 pathway activation was comparable in slow-growing ρ xenografts and rapid-growing parental xenografts. Interestingly, we found that ex vivo ρ cells derived from ρ xenografts exhibited slightly increased HIF-1α expression and modest HIF-1 pathway activation regardless of oxygen concentration. Surprisingly, ρ cells, as well as parental cells treated with oxidative phosphorylation inhibitors, were unable to boost HIF-1 transcriptional activity during hypoxia, although HIF- 1α protein levels were ordinarily increased in these cells under hypoxic conditions. These findings indicate that mitochondrial deficiency causes loss of hypoxia-induced HIF-1 transcriptional activity and thereby might lead to a constitutive HIF-1 pathway activation as a cellular adaptation mechanism in tumor microenvironment.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85012870600&origin=inward; http://dx.doi.org/10.18632/oncotarget.14415; http://www.ncbi.nlm.nih.gov/pubmed/28060746; https://www.oncotarget.com/lookup/doi/10.18632/oncotarget.14415; https://dx.doi.org/10.18632/oncotarget.14415; https://www.oncotarget.com/article/14415/text/
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