In Cancer Research this week, researchers in Italy and France report that expression of the P2X7 receptor can increase tumor growth in vivo. P2X7 is usually known for being cytotoxic, but recent evidence has shown it plays a role in cell proliferation as well, the authors write. For this study, they found that P2X7 exhibits significant growth-promoting effects in vivo, and that human embryonic kidney cells expressing P2X7 exhibit a more tumorigenic and anaplastic phenotype than control cells. Further, the team adds, "the growth rate and size of these tumors were significantly reduced by intratumoral injection of the P2X7 inhibitor — oxidized ATP."
Also in Cancer Research this week, researchers at the University of Pittsburgh Cancer Institute report that cell-mediated autophagy promotes cancer cell survival. The team examined individual target cells after exposure to lymphoid effectors, and found that human peripheral blood lymphocytes provide lytic signals and also promote autophagy in the remaining cells. "At high effector-to-target ratios, autophagy was induced in several human tumors, as assessed by induction of LC3 puncta and diminished p62," the team writes. "Natural killer cells are a primary mediator of this process. In addition, target cell autophagy was enhanced by provision of interleukin (IL)-2, whereas IL-10 attenuated this effect, and cell-to-cell contact strongly enhanced lymphocyte-mediated autophagy."
Finally in Cancer Research this week, researchers in the US and South Korea describe a novel TOPK inhibitor that effectively suppresses the growth of colon cancer. Using an in vitro kinase assay, the team screened 36 drug candidates and identified HI-TOPK-032 — a compound that strongly suppresses TOPK kinase activity in vitro, but had little effect on the kinase activities of ERK1, c-jun-NH2-kinase 1, or p38. "HI-TOPK-032 also inhibited anchorage-dependent and -independent colon cancer cell growth by reducing ERK-RSK phosphorylation as well as increasing colon cancer cell apoptosis through regulation of the abundance of p53, cleaved caspase-7, and cleaved PARP," the team writes. Further, in a xenograft model of colon cancer, the compound suppressed tumor growth.