Activation of Toll-like receptor 7 regulates the expression of IFN-λ1, p53, PTEN, VEGF, TIMP-1 and MMP-9 in pancreatic cancer cells.

Toll-like receptors (TLRs) are critical in the induction of the immune response in tumor development. TLR7 has previously been demonstrated to be associated with the development of pancreatic cancer, and the release of cytokines and chemokines from other types of cancer cell; however, the specific expression induced by TLR7 agonists in pancreatic cancer cells remains to be elucidated. The present study aimed to investigate the effects of the TLR7 agonist, gardiquimod, on ERK1/2 signaling pathway, and on the expression of genes involved in the pathogenesis of cancer, including phosphatase and tensin homolog deleted on chromosome 10 (PTEN), p53, type Ⅲ interferon (IFN-λ1), vascular endothelial growth factor (VEGF), matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1).

Activation of Toll-like receptor 7 inhibits the proliferation and migration, and induces the apoptosis of pancreatic cancer cells.

Pancreatic cancer is one of the most malignant types of tumor and has a poor prognosis. Toll‑like receptor 7 (TLR7) has been found to be present and have different roles in different types of cancer cells. In the present study, the roles of TLR7 in BxPC‑3 cells, a human pancreatic adenocarcinoma cell line, were investigated.

CXCR4 antagonist AMD3100 modulates claudin expression and intestinal barrier function in experimental colitis.

Ulcerative colitis is a gastrointestinal disorder characterized by local inflammation and impaired epithelial barrier. Previous studies demonstrated that CXC chemokine receptor 4 (CXCR4) antagonists could reduce colonic inflammation and mucosal damage in dextran sulfate sodium (DSS)-induced colitis. Whether CXCR4 antagonist has action on intestinal barrier and the possible mechanism, is largely undefined.