Design of dendrimer modified carbon nanotubes for gene delivery
- 123 Downloads
To investigate the efficiency of polyamidoamine dendrimer grafted carbon nanotube (dendrimer-CNT) mediated entrance of anti-survivin oligonucleotide into MCF-7 cells, and its effects on the growth of MCF-7 cells.
Antisense survivin oligonucleotide was anchored onto polyamidoamine dendrimer grafted carbon nanotubes to form dendrimer-CNT-asODN complex and the complex was characterized by Zeta potential, AFM, TEM, and 1% agarose gel electrophoresis analysis. Dendrimer-CNT-asODN complexes were added into the medium and incubated with MCF-7 cells. MTT method was used to detect the effects of asODN and dendrimer-CNT-asODN on the growth of MCF-7 cells. TEM was used to observe the distribution of dendrimer-CNT-asODN complex within MCF-7 cells.
Successful synthesis of dendrimer-CNT-asODN complexes was proved by TEM, AFM and agarose gel electrophoresis. TEM showed that the complexes were located in the cytoplasm, endosome, and lysosome within MCF-7 cells. When dendrimer-CNT-asODN (1.0 μmol/L) and asODN (1.0 μmol/L) were used for 120 h incubation, the inhibitory rates of MCF-7 cells were (28.22±3.5)% for dendrimer-CNT-asODN complex group, (9.23±0.56)% for only asODN group, and (3.44±0.25)% for dendrimer-CNT group. Dendrimer-CNT-asODN complex at 3.0 μmol/L inhibited MCF-7 cells by (30.30±10.62)%, and the inhibitory effects were in a time-and concentration-dependent manner.
Dendrimer-CNT nanoparticles may serve as a gene delivery vector with high efficiency, which can bring foreign gene into cancer cells, inhibiting cancer cell proliferation and markedly enhancing the cancer therapy effects.
Key wordsGene delivery Carbon nanotube Polyamidoamine dendrimer Cancer therapy Survivin gene
Unable to display preview. Download preview PDF.
- Yamamoto T, Manome Y, Nakamura M, et al. Downregulation of survivin expression by induction of the effector cell protease receptor-1 reduces tumor growth potential and results in an increased sensitivity to anticancer agents in human colon cancer [J]. Eur J Cancer 2002; 38:2316–24.PubMedCrossRefGoogle Scholar