In BMC Cancer this week, researchers in Italy and the US say that glioblastoma-derived leptin induces tube formation and growth of endothelial cells in the disease, and compared that with the effects of VEGF on glioblastoma. Leptin has been implicated in the formation and progression of glioblastoma; the hormone and its receptor are over-expressed relative to the surrounding normal tissue, the authors write. Using in vitro models, the team found that glioblastoma cell lines LN18 and LN229 express leptin mRNA and that LN18 cells secrete detectable amounts of leptin protein. Both lines also express VEGF. "Our data provide the first evidence that LN18 and LN 229 human glioblastoma multiforme cells … might produce biologically active leptin, which can stimulate tube formation and enhance proliferation of endothelial cells," the researchers write. "Furthermore, we demonstrate for the first time that a peptide ObR antagonist inhibits proangiogenic and growth effects of leptin on endothelial cells, and that the pharmacological potential of this compound might be combined with drugs targeting the VEGF pathway."
Also in BMC Cancer this week, researchers in Germany study the presence of fatty acid binding proteins in prostate, bladder, and kidney cancer, and suggest that IL-FABP could be used as a predictor of survival in patients with renal cell carcinoma. The team analyzed nine cell lines of renal carcinomas, seven of urinary bladder carcinomas, and five of prostate carcinomas, and found "distinctly different" FABP expression patterns between the cell lines of the different cancers as well as within the cell lines from the same cancer. "The FABP patterns in the cell lines do not always reflect the real situation in the tumors," the authors write. "These facts have to be considered in functional studies concerning the different FABPs." In addition, the team saw that IL-FABP was over-expressed in renal tumor tissue, and identified the ratio as "an independent indicator of survival outcome."
And finally in BMC Cancer this week, researchers in Norway say that cyclic AMP induces apoptosis in multiple myeloma cells and inhibits tumor development in mice. The team used both murine and human multiple myeloma cell lines and treated them with cAMP elevating agents and cAMP analogs. Forskolin, a cAMP elevating agent, more than tripled the number of cells that died in the murine cell line MOPC315 and human cell lines U266 and INA-6. The authors write that "cAMP-mediated cell death had all the typical hallmarks of apoptosis, including changes in the mitochondrial membrane potential and cleavage of caspase 3, caspase 9 and PARP. Forskolin also inhibited the growth of multiple myeloma cells in a mouse model in vivo." This suggests, the team adds, that compounds activating the cAMP signaling pathway might be useful in combating multiple myeloma.