In Cancer Cell this week, researchers in Germany and Switzerland report that endothelial CCR2 signaling induced by colon cancer cells enables the metastasis of those cells through the JAK2-Stat5 and p38MAPK pathway. Increased expression of CCL2 in colon tumor cells correlates with enhanced metastasis, poor prognosis, and the recruitment of CCR2+Ly6Chi monocytes, the team says. In this study, the researchers demonstrate that tumor cell-derived CCL2 in metastatic stage IV colon carcinomas "activates the CCR2+ endothelium to increase vascular permeability in vivo." They also found that a reduction of CCR2 expression decreased metastasis, but didn't prevent it, and that CCL2-induced vascular permeability and metastasis "is dependent on JAK2-Stat5 and p38MAPK signaling."
Also in Cancer Cell this week, researchers in Japan report that Nrf2 is involved in redirecting glucose and glutamine to cancer cells. "Here, we show that Nrf2 redirects glucose and glutamine into anabolic pathways, especially under the sustained activation of PI3K-Akt signaling," the team writes. "The active PI3K-Akt pathway augments the nuclear accumulation of Nrf2 and enables Nrf2 to promote metabolic activities that support cell proliferation in addition to enhancing cytoprotection."