Regression of established subcutaneous B16‐F10 murine melanoma tumors after gef gene therapy associated with the mitochondrial apoptotic pathway

Abstract

Novel treatment modalities, including gene therapy, are needed for patients with advanced melanoma. We evaluated whether the gef gene, a suicide gene from Escherichia coli, had a significant cytotoxic impact on melanoma in vivo. First, we used a non-viral gene delivery approach (pcDNA3.1/gef) to study the inhibition of melanoma cells (B16-F10) proliferation in vitro. Secondly, we used direct intra-tumoral injection of pcDNA3.1/gef complexed with jetPEI to deliver gef cDNA to rapidly growing murine melanomas. We demonstrated that gef gene not only has an antiproliferative effect on B16-F10 cells in vitro, but also induces an important decrease in melanoma tumor volume (77.7% in 8 days) in vivo. Interestingly, after gef gene treatment, melanoma showed apoptosis activation associated with the mitochondrial pathway, suggesting that the induction of this death mechanism may be an effective strategy for its treatment. Our in vivo results indicate that gef gene might become a suitable therapeutic strategy for patients with advanced melanoma.

Dexmedetomidine attenuates LPS‐mediated BV2 microglia cells inflammation via inhibition of glycolysis

“…It was reported that augment of glycolysis in microglia participates in microglial inflammation . Glycolysis pathway activation offers fundamental biomacromolecule, including amino acids and fatty acids to synthetize inflammatory mediators in immunocytes . Similarly, the present study indicated that glycolysis pathway activation participated in microglia inflammation ( Figures , ).…”

Subcutaneous Adipocytes Promote Melanoma Cell Growth by Activating the Akt Signaling Pathway

“…B16F10 (5 ϫ 10 5 ) cells were first treated (21) with palmitic acid (6 M) in 1% fatty acid-free BSA for 24 h. B16F10 cells treated with 1% fatty acid-free BSA were used as a control. Tumors were then induced by subcutaneous injection of the 5 ϫ 10 5 palmitic acid-treated B16F10 or control B16F10 cells into the left flanks of C57 mice (21,22). Body weight was measured every day.…”

Characterization and longitudinal monitoring of melanoma growth in ret‐transgenic mice using a single‐sequence MRI protocol

“…Animal models serve to provide us with a better understanding of basic disease pathogenesis and the effects of therapeutic agents. In the field of dermato‐oncological research, immunodeficient mice are frequently used to host human tumor cells . A major drawback of these models is the so‐called ‘species barrier’ and the fact that the use of immunodeficient animals might influence the results .…”