Apatinib Promotes Apoptosis of Pancreatic Cancer Cells through Downregulation of Hypoxia-Inducible Factor-1α and Increased Levels of Reactive Oxygen Species.
Ke HeLu WuQianshan DingFarhan HaiderHonggang YuHaihe WangGuoan XiangPublished in: Oxidative medicine and cellular longevity (2019)
At present, apatinib is considered a new generation agent for the treatment of patients with gastric cancer. However, the effects of apatinib on pancreatic cancer have not been clarified. This study investigated the impact of apatinib on the biological function of pancreatic cancer cells and the potential mechanism involved in this process. Using the Cell Counting Kit-8 method, we confirmed that apatinib treatment inhibited cell proliferation in vitro. Moreover, the migration rate of pancreatic cells was inhibited. The effects of apatinib on apoptosis and cell cycle distribution of pancreatic carcinoma cells were detected by flow cytometry. The number of apoptotic cells was significantly increased, and the cell cycle was altered. Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro. Apatinib significantly inhibited the biological function of pancreatic cancer cells. It promoted apoptosis, downregulated the expression of HIF-1α, and increased the levels of reactive oxygen species.
Keyphrases
- cell cycle
- cell cycle arrest
- cell proliferation
- reactive oxygen species
- pi k akt
- cell death
- induced apoptosis
- endoplasmic reticulum stress
- signaling pathway
- vascular endothelial growth factor
- oxidative stress
- poor prognosis
- endothelial cells
- stem cells
- binding protein
- single cell
- tyrosine kinase
- mass spectrometry
- replacement therapy
- anti inflammatory
- human health