Mcam Silencing With RNA Interference Using Magnetofection has Antitumor Effect in Murine Melanoma
Year: 2014
Type: article
Abstract: The melanoma cell adhesion molecule (MCAM) is involved in melanoma development and its progression, including invasiveness, metastatic potential and angiogenesis. Therefore, MCAM represents a potential target for gene therapy of melanoma, whose expression could be hindered with posttranscriptional specific gene silencing with RNA interference technology. In this study, we constructed a plasmid DNA encoding short hairpin RNA against MCAM (pMCAM) to explore the antitumor and antiangiogenic effects. The experiments were performed in vitro on murine melanoma and endothelial cells, as well as in vivo on melanoma tumors in mice. The antiproliferative, antimigratory, antiangiogenic and antitumor effects were examined after gene therapy with pMCAM. Gene delivery was performed by magnetofection, and its efficacy compared to gene electrotransfer. Gene therapy with pMCAM has proved to be an effective approach in reducing the proliferation and migration of melanoma cells, as well as having antiangiogenic effect in endothelial cells and antitumor effect on melanoma tumors. Magnetofection as a developing nonviral gene delivery system was effective in the transfection of melanoma cells and tumors with pMCAM, but less efficient than gene electrotransfer in in vivo tumor gene therapy due to the lack of antiangiogenic effect after silencing Mcam by magnetofection.
DOI: 10.1038/mtna.2014.56
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,900
Awards: Antiangiogena genska terapija raka: tarčno zdravljenje z uporabo elektroporacije in magnetnih nanodelcev kot dostavnih sistemov (Slovene), Priprava in validacija terapevtskih plazmidov brez selekcijskega gena za antibiotično rezistenco za gensko terapijo raka z inducibilnimi in tkivno specifičnimi promotorji (Slovene), Development and evaluation of new approaches to cancer treatment
OpenAlex ID: W2010313871
