Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell

Autor: Guowen Li, Sai-Nan Zeng, Manping Huang, Bin Huang
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
MAPK/ERK pathway
KDR (VEGFR2)
MAP Kinase Signaling System
Pyridines
RAF/MEK/ERK pathway
Cell
Antineoplastic Agents
Cholangiocarcinoma
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Cell Movement
Cell Line
Tumor
medicine
Humans
Apatinib
Neoplasm Invasiveness
lcsh:RC799-869
Protein kinase B
Protein Kinase Inhibitors
PI3K/AKT/mTOR pathway
Cell Proliferation
Phosphoinositide-3 Kinase Inhibitors
business.industry
Cell growth
Gastroenterology
Cell migration
General Medicine
Vascular Endothelial Growth Factor Receptor-2
VEGF
Vascular endothelial growth factor
PI3K/AKT pathway
030104 developmental biology
medicine.anatomical_structure
chemistry
Bile Duct Neoplasms
030220 oncology & carcinogenesis
Cancer research
cardiovascular system
raf Kinases
lcsh:Diseases of the digestive system. Gastroenterology
business
Proto-Oncogene Proteins c-akt
Research Article
Zdroj: BMC Gastroenterology, Vol 18, Iss 1, Pp 1-10 (2018)
BMC Gastroenterology
DOI: 10.1186/s12876-018-0870-3
Popis: Background Cholangiocarcinoma (CCA) is a form of cancer that easily aggress to contiguous structures. Vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2) are increased in majority species of cancers and suppress tumor progression by blocking VEGF/VEGFR2. Apatinib is a highly selective VEGFR2 antagonist which has inhibitive effect on antiapoptotic and cell growth in CCA. While, the effect of apatinib cell migration and invasion in CCA is still unknown. Methods CCA cell lines QBC939 and TFK-1 were transfected with siKDR to establish the KDR function loss cell model, and recombined human VEGF (rhVEGF) protein was added into the culture medium to enhance the VEGF expression. RT-qPCR and western bloting were used to detect the mRNA and protein expression levels of VEGFR2 to investigate whether it was effectively repressed or activated with rhVEGF or apatinib treatment. Then, MTT, wound healing assay, and transwell matrix assay were applied to measure the effect of apatinib and rhVEGF on cell viability, migration and invasion, respectively. Results The mRNA and protein expressions of VEGFR2 were significantly reduced with KDR RNAi in both QBC939 and TFK-1 cells, and rhVEGF treatment increased these expression levels (p
Databáze: OpenAIRE
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