Data from: Downregulation of sST2, a decoy receptor for interleukin-33, enhances subcutaneous tumor growth in murine pancreatic cancer cells

Despite the recent scientific advancements, pancreatic cancer remains the
7th leading cause of cancer-related mortality. Pancreatic cancer
progression is closely associated with inflammation, and we previously
showed that short hairpin RNA–mediated knockdown of sST2 expression, a
soluble decoy receptor for the proinflammatory molecule interleukin-33
(IL-33), in mouse Panc02 pancreatic cancer cells reduced malignant growth
following pancreatic (orthotopic) implantation. Furthermore, this growth
suppression was accompanied by decreased tumor angiogenesis, reduced
expression of the neutrophil chemoattractant CXCL3, and a lower number of
tumor-associated neutrophils (TANs). In contrast to previous results, in
this study, we showed that IL-33-dependent tumor growth and pulmonary
metastasis occurred following subcutaneous (ectopic) implantation of
sST2-knockdown cells. This was associated with a decrease in the levels of
the anti-inflammatory molecule adiponectin and the number of
GLUT4-positive cancer-associated adipocytes, as well as an increase in
IκBα phosphorylation levels, Cxcl3 expression, and the accumulation of
infiltrating CD206+ protumor N2 TANs. Taken together, these results
suggest that Panc02 cell-derived sST2 differentially affects malignant
growth in the tumor microenvironment depending on the implantation site.