Neurotensin, a gut tridecapeptide, acts as a potent cellular mitogen for various colorectal and pancreatic cancers which possess high-affinity neurotensin receptors (NTR).

Neurotensin induces the expression of MIP-2, MCP-1, IL-1β and TNFα in murine microglial cells and stimulates IL-8 secretion in a non-transformed colon epithelial cell line stably transfected with the NTR. The high-affinity NTR, a member of the G-protein coupled receptor (GPCR) family, is present in a majority of human pancreatic and colorectal cancers, suggesting that Neurotensin (NT) may act in an endocrine fashion to affect tumor growth. Acting through the NTR1, Neurotensin is known to stimulate various signal transduction pathways, including intracellular calcium ([Ca²⁺]_i), the mitogen-activated protein kinases (MAPKs), ERK and JNK, and various PKC isoforms. Treatment of HCT116 cells with Neurotensin (100 nM) significantly increases HCT116 cell migration (~3-fold) compared with vehicle treatment; pretreatment with Curcumin (10 μM) blocksthe stimulatory effect of NT on HCT116 cell migration. ctivation of MEK/ERK by NT and downstream induction of AP-1 transcription factors contributes to the proliferative effects of Neurotensin.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Wang X, et al. Curcumin inhibits neurotensin-mediated interleukin-8 production and migration of HCT116 human colon cancer cells. Clin Cancer Res. 2006 Sep 15;12(18):5346-55.  [Content Brief]