Episomal Lentiviral Vector-Mediated miR-145 Overexpression Inhibits Proliferation and Induces Apoptosis of Human Esophageal Carcinomas Cells.
Recent Pat Anticancer Drug Discov
; 11(4): 453-460, 2016.
Article
en En
| MEDLINE
| ID: mdl-27549139
ABSTRACT
BACKGROUND:
Gene therapy is a promising approach for the treatment of various cancers. However, most viral vectors used for this purpose carry risks, including potential integration into the host genome.OBJECTIVE:
We addressed this issue in the present study by constructing an episomal lentiviral vector using the .-interferon matrix attachment region to express the microRNA -145(miR-145), and examining the effect of miR-145 overexpression on human esophageal carcinomas (EC) cells. Some recent relevant patents are also discussed.METHOD:
Expression levels of miR-145 and the marker protein enhanced green fluorescent protein (EGFP) in infected ECA109 and EC9706 human esophageal carcinoma cells were detected by quantitative PCR and flow cytometry, respectively. Cell proliferation and apoptosis were assessed by Cell Counting Kit-8 and flow cytometry, respectively. Plasmid rescue experiments and fluorescence in situ hybridization were used to determine the episomal status of the transfected vector.RESULTS:
We found that EGFP and miR-145 were highly expressed in EC cells, and miR-145 overexpression inhibited cell proliferation and induced apoptosis. Moreover, the lentiviral vector did not integrate into the host genome, but was maintained episomally at lower copy numbers.CONCLUSION:
Taken together, our results demonstrate that miR-145-expressing episomal lentiviral vectors are a promising tool for gene therapy in the treatment of EC.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Plásmidos
/
Neoplasias Esofágicas
/
Carcinoma
/
Terapia Genética
/
Apoptosis
/
Lentivirus
/
MicroARNs
/
Proliferación Celular
/
Vectores Genéticos
Límite:
Humans
Idioma:
En
Revista:
Recent Pat Anticancer Drug Discov
Asunto de la revista:
NEOPLASIAS
/
TERAPIA POR MEDICAMENTOS
Año:
2016
Tipo del documento:
Article