Apatinib regulates the cell proliferation and apoptosis of liver cancer by regulation of VEGFR2/STAT3 signaling
| Autor: | Jun Luo, Jiaping Zheng, Guoliang Shao, Danlin Gu, Song Wen, Hui Zeng |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
STAT3 Transcription Factor Vascular Endothelial Growth Factor A Cell Survival Pyridines Antineoplastic Agents Apoptosis Pathology and Forensic Medicine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell Line Tumor medicine Humans Apatinib STAT3 Cell Proliferation biology Chemistry Cell growth Liver cell Liver Neoplasms Kinase insert domain receptor Cell Biology medicine.disease Vascular Endothelial Growth Factor Receptor-2 Vascular endothelial growth factor 030104 developmental biology 030220 oncology & carcinogenesis Cancer research biology.protein Liver cancer Signal Transduction |
| Zdroj: | Pathology, research and practice. 215(4) |
| ISSN: | 1618-0631 |
| Popis: | Liver cancer is the third most common cause of cancer related death worldwide. Apatinib showed satisfactory efficacy in various types of cancers, including breast cancer, malignant fibrous histiocytoma and liver cancer. However, how did Apatinib function in liver cancer is largely unknown. mRNA levels of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR2) as well as protein levels of VEGF and p-VEGFR2 were obviously higher in liver cancer cell line SMCC7721 than in normal liver cell LO2. Apatinib significantly inhibited the mRNA levels of VEGF and VEGFR2 as well as protein levels of VEGF and p-VEGFR2 compared with those in control group. At 12, 24 and 48 h after corresponding treatments, compared with the control group, Apatinib significantly lowered the cell viability of SMCC7721 cells, while transfection of si-signal transducer and activator of transcription 3 (siSTAT3) further augmented the effects of Apatinib. At 48 h after treatment, compared with the control group, Apatinib significantly upregulated the cell apoptosis rate of SMCC7721 cells, which was further induced by the transfection of siSTAT3. Compared with control group, Apatinib significantly induced BAX/Bcl-2 ratio elevation, reduced p-STAT3 and p-VEGFR2 expression, which were significantly augmented by the treatment of siSTAT3. In conclusion, Apatinib inhibited the cell proliferation and promoted the cell apoptosis of liver cancer by inhibiting the activation of VEGFR2/STAT3. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect