ArticleOncology letters2017
Regulation of angiogenic factors by the PI3K/Akt pathway in A549 lung cancer cells under hypoxic conditions.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Cytotoxic Effects of Medicinal Plant Extracts on HeLa Cells via Redox Imbalance, L-Arginine Metabolic Reprogramming, and Glycolytic Suppression.Cell biochemistry and function · 2026Article
- Aryl hydrocarbon receptor-dependent lipid droplet accumulation supports redox homeostasis in hypoxia-induced PCa cells.American journal of cancer research · 2026Article
- The potential of miR-29 in modulating tumor angiogenesis: a comprehensive review.Discover oncology · 2025Review
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- Beyond Conventional: The New Horizon of Anti-Angiogenic microRNAs in Non-Small Cell Lung Cancer Therapy.International journal of molecular sciences · 2020Review
- Poly(1-vinylimidazole) polyplexes as novel therapeutic gene carriers for lung cancer therapy.Beilstein journal of nanotechnology · 2020Article
- Cytochalasin H Inhibits AngiogenesisJournal of Cancer · 2019Article
- [Research Advances of Ang-2 in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018Review
- Intranasal administration of nerve growth factor promotes angiogenesis via activation of PI3K/Akt signaling following cerebral infarction in rats.American journal of translational research · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the influence of hypoxia and PI3K inhibition on angiogenic factors in A549 lung cancer cells. A549 cells were treated with the PI3K inhibitor LY294002 under normoxic and hypoxic conditions. Untreated cells were used as the control group and those treated by the inhibitor, as the suppression group. The cells were further divided based on normoxic or hypoxic conditions and named: Normoxic control group, normoxic suppression group, hypoxic control group and hypoxic suppression group. Expression levels of hypoxia-inducible factor (HIF)-1α and AKT1 mRNA in all groups were determined by reverse transcriptase-quantitative polymerase chain reaction and concentrations of vascular endothelial growth factor (VEGF), angiotensin II (ANG-II), transforming growth factor (TGF)-α/β1, and tumor necrosis factor (TNF)-α in the culture supernatant were measured by enzyme-linked immunosorbent assay. The expression levels of HIF-1α and AKT1 mRNA in the hypoxic control group were higher than those in the normoxic control group and the expression levels of HIF-1α and AKT1 mRNA in the hypoxic control group were higher than those in the hypoxic suppression group. Compared to the normoxic control and normoxic suppression groups, the concentrations of VEGF and TNF-α in supernatant were higher in the hypoxic control and hypoxic suppression groups, respectively. However, TGF-α and TGF-β1 demonstrated the opposite trend of the aforementioned factors. The concentration of ANG-II in the hypoxic suppression group was higher than that in the normoxic suppression group. In addition, compared to the normoxic control group and hypoxic control group, the concentrations of VEGF and TGF-β1 in supernatant were lower in the normoxic suppression group and in the hypoxic suppression group, respectively. In conclusion, the results of the present study suggest that hypoxia can stimulate A549 lung cancer cells to secrete VEGF and TNF-α and inhibit TGF-α and TGF-β1. The ability of A549 cells to secrete VEGF and TGF-β1 is regulated by PI3K/Akt, and ANG-II expression may be regulated by the PI3K/Akt pathway under hypoxic condition.
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