In Cancer Cell this week, researchers in China and Massachusetts say the production of the cytokine CCL18 from tumor-associated macrophages promotes breast cancer metastasis via the PITPNM3 receptor. Breast tumor-associated macrophages produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced survival, the authors write. CCL18 promotes the invasiveness of cancer cells by "triggering integrin clustering and enhancing their adherence to extracellular matrix," they add. "Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling."
Also in Cancer Cell this week, researchers in Germany and Japan say the activation of the Stat3 and Scocs3 genes by IL6 trans-signaling promotes progression of pancreatic intraepithelial neoplasia and the development of pancreatic cancer. "The myeloid compartment induces Stat3 activation by secreting IL-6; consequently, IL-6 trans-signaling activates Stat3 in the pancreas," the authors write. "Aberrant activation of Stat3 through homozygous deletion of Socs3 in the pancreas accelerates pancreatic intraepithelial neoplasia progression and pancreatic ductal adenocarcinoma development."
Finally in Cancer Cell this week, researchers in Pennsylvania and Tennessee present findings on the role of p120-catenin in the development of cancer. No proof has emerged to date that p120-catenin acts as a tumor suppressor gene, however loss of p120-catenin does lead to tumor development in mice, the authors write. The team generated a conditional knockout model of p120-catenin and found that mice without the gene develop preneoplastic and neoplastic lesions in the oral cavity, esophagus, and squamous forestomach.