Inhibition of VEGF expression and SMMC 7721 cell growth by VEGFsiRNA
Huan Zhang
Abstract
Huan Zhang
Abstract
AIM: To determine the inhibition of VEGF small interfering RNA (siRNA) on expression of VEGF protein and SMMC 7721 cell growth. METHODS: Nine VEGFsiRNA sequences with nineteen nucleotides were designed under the assistance of computer. The inhibitory effect of VEGFsiRNA was analyzed by CCK8. The protein level of VEGF in the media was determined by ELISA. The change of cell cycle was detected by flow cytometry. RESULTS: All the VEGFsiRNA were capable of inhibiting the proliferation of SMMC 7721 cells significantly compared with control and lipofectamine control, while the inhibitory effects of VEGFsiRNA2, VEGFsiRNA4, VEGFsiRNA6, VEGFsiRNA7, VEGFsiRNA8 and VEGFsiRNA9 were better than that of antisense oligodeoxynucleotide. All the VEGFsiRNA reduced the expression of VEGF protein. The effect of VEGFsiRNA7 and VEGFsiRNA2 were the best with the inhibitory rates of 52.65% and 50.43%, respectively. VEGFsiRNAs induced the S arrest in SMMC 7721 cells. The signs of apoptosis in SMMC 7721 cells induced by VEGFsiRNA were not observed. CONCLUSION: VEGFsiRNA sequences were designed and synthesized successfully. VEGFsiRNA effectively inhibited the proliferation of SMMC 7721 cells and reduced the level of VEGF protein.
OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
AIM: To determine the inhibition of VEGF small interfering RNA (siRNA) on expression of VEGF protein and SMMC 7721 cell growth. METHODS: Nine VEGFsiRNA sequences with nineteen nucleotides were designed under the assistance of computer. The inhibitory effect of VEGFsiRNA was analyzed by CCK8. The protein level of VEGF in the media was determined by ELISA. The change of cell cycle was detected by flow cytometry. RESULTS: All the VEGFsiRNA were capable of inhibiting the proliferation of SMMC 7721 cells significantly compared with control and lipofectamine control, while the inhibitory effects of VEGFsiRNA2, VEGFsiRNA4, VEGFsiRNA6, VEGFsiRNA7, VEGFsiRNA8 and VEGFsiRNA9 were better than that of antisense oligodeoxynucleotide. All the VEGFsiRNA reduced the expression of VEGF protein. The effect of VEGFsiRNA7 and VEGFsiRNA2 were the best with the inhibitory rates of 52.65% and 50.43%, respectively. VEGFsiRNAs induced the S arrest in SMMC 7721 cells. The signs of apoptosis in SMMC 7721 cells induced by VEGFsiRNA were not observed. CONCLUSION: VEGFsiRNA sequences were designed and synthesized successfully. VEGFsiRNA effectively inhibited the proliferation of SMMC 7721 cells and reduced the level of VEGF protein.
Key concepts: Lipofectamine, Flow cytometry, Cell growth, Apoptosis, Molecular biology, Inhibitory postsynaptic potential, Small interfering RNA, Cell cycle