Abstract

Objective To explore the expression of vascular endothelial growth factor (VEGF) in glioblastoma cells after silencing the oncogene c-myc through RNA interference (RNAi). Methods The shRNA interference plasmid named pCMYC targeting c-myc gene and the pHK plasmid as negative control were constructed. The expression of c-myc and VEGF mRNA and protein was detected by using reverse transcription-polymerase chain reaction (RT-PCR), immunocytochemistry and Western blotting among different groups. Results ( 1 ) The mRNA expression of c-myc and VEGF in IN500Δ-pCMYC cells (0. 273 ±0. 028, 0. 443 ±0. 048) was lower than that of IN500Δ ( 1. 185 ±0. 145, 1. 116 ±0. 072) and IN500Δ-pHK cells ( 1. 098 t0. 128, 1. 208 ±0. 133) (P <0. 01 ) ; (2) Immunocytochemical staining revealed that the expression of c-myc and VEGF protein in IN500Δ-pCMYC cells was lower than in IN500Δ cells and IN500Δ-pHK cells (P<0. 05); (3) Western blotting indicated that the expression of c-myc and VEGF protein in IN500Δ-pCMYC cells (0. 221 ± 0. 041, 0. 284 ± 0. 025 ) was lower than that in IN500Δ cells (1.821±0.191, 1.531 ±0.213) and IN500A-pHK cells (1.650±0.110, 1.820±0.122) (P<0. 01 ). Conclusion Sliencing the expression of c-myc oncogene could effectively inhibit the expression of VEGF. Key words: c-myc gene; RNA interference; Vascular endothelial growth factor; Glioma

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.