Abstract
Neuropilin-1 (NRP-1) is a novel receptor of vascular endothelial growth factor 165 that promotes angiogenesis, tumor growth, tumor invasion and metastasis. However, its role in tumorigenesis and progression of human hepatocellular carcinoma (HCC) is unknown. In this study, lentivirus-mediated short hairpin RNA (shRNA) was used to silence NRP-1 in the HCCLM6 cell line to explore its role in regulating the growth of HCC. Recombinant NRP-1 shRNA lentivirus was prepared and transfected into HCCLM6 cells. Transfection efficiencies of the lentivirus were observed by flow cytometry. Protein and mRNA expression of NRP-1 were examined by western blot analysis and quantitative reverse transcription-polymerase chain reaction (RT-PCR), and the effect of the lentivirus on cell growth was determined using MTT assay. Different cell groups were inoculated into nude mice to establish cancer xenografts, and tumor growth was monitored. Protein expression of NRP-1 in tumor tissues was detected by western blot assay. Microvessel density (MVD) in tumor tissues was assessed by immunohistochemistry (IHC). Lentivirus-mediated shRNA efficiently reduced endogenous NRP-1 expression in HCCLM6 cells and significantly inhibited cell growth in vitro. In vivo, NRP-1 knockdown in tumor tissues resulted in decreased vasculature. NRP-1 promotes the growth of HCC in vitro and in vivo, and therefore may be considered as a novel therapeutic target for HCC.
Highlights
Introduction of treatment failure and cancer mortalities
NRP‐1 was found to be a co‐receptor for vascular endothelial growth factor 165 (VEGF 165) and is expressed in endothelial cells (EC), where it is involved in the regulation of angiogenesis and endothelial cell migration [7,8,9]
The real‐time PCR results demonstrated that NRP‐1 short hairpin RNA (shRNA) had a significant suppressive effect
Summary
Introduction of treatment failure and cancer mortalities. Angiogenesis is essential for the growth, invasion and metastasis of solid tumors. Overexpression of NRP‐1 in a transgenic mouse model increased capillary and blood vessel formation and resulted in hemorrhage [10], whereas functional inactivation of NRP‐1 in mice led to embryonic lethality with multiple vascular abnormalities, including of avascular regions, heterogeneous blood vessel size and abnormally formed dorsal aorta [11]. These results indicated that NRP‐1 was a key regulator of developmental angiogenesis. Even with improvement in surgical procedures and other adjuvant therapies, rapid growth, high recurrence and metastasis are still the main cause
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