G-protein-coupled receptors mediate ω-3 PUFAs-inhibited colorectal cancer by activating the Hippo pathway

Oncotarget. 2016 Sep 6;7(36):58315-58330. doi: 10.18632/oncotarget.11089.

Abstract

Colorectal cancer (CRC) is one of the most common cancers leading to high mortality. However, long-term administration of anti-tumor therapy for CRC is not feasible due to the side effects. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), particularly DHA and EPA, exert protection against CRC, but the mechanisms are unclear. Here, we show that ω-3 PUFAs inhibit proliferation and induce apoptosis of CRC cells in vitro and alleviate AOM/DSS-induced mice colorectal cancer in vivo. Moreover, ω-3 PUFAs promote phosphorylation and cytoplasmic retention of YAP and this effect was mediated by MST1/2 and LATS1, suggesting that the canonical Hippo Pathway is involved in ω-3 PUFAs function. We further confirmed that increase of pYAP by ω-3 PUFAs was mediated by GPRs, including GPR40 and GPR120, which subsequently activate PKA via Gαs, thus inducing the Hippo pathway activation. These data provide a novel DHA/EPA-GPR40/120-Gαs-PKA-MST1/2-LATS1-YAP signaling pathway which is linked to ω-3 PUFAs-induced inhibition of cell proliferation and promotion of apoptosis in CRC cells, indicating a mechanism that could explain the anti-cancer action of ω-3 PUFAs.

Keywords: GPR; Hippo pathway; YAP; colorectal cancer; omega-3 PUFAs.

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis
  • Azoxymethane / chemistry
  • Cell Cycle Proteins
  • Cell Line, Tumor
  • Cell Proliferation
  • Colorectal Neoplasms / metabolism*
  • Colorectal Neoplasms / therapy
  • Cytoplasm / metabolism
  • Dextran Sulfate / chemistry
  • Fatty Acids, Omega-3 / metabolism*
  • HT29 Cells
  • Hippo Signaling Pathway
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Phosphoproteins / metabolism
  • Phosphorylation
  • Protein Serine-Threonine Kinases / metabolism*
  • Protein Transport
  • Receptors, G-Protein-Coupled / metabolism*
  • YAP-Signaling Proteins

Substances

  • Adaptor Proteins, Signal Transducing
  • Antineoplastic Agents
  • Cell Cycle Proteins
  • Fatty Acids, Omega-3
  • Phosphoproteins
  • Receptors, G-Protein-Coupled
  • YAP-Signaling Proteins
  • Yap1 protein, mouse
  • Dextran Sulfate
  • Protein Serine-Threonine Kinases
  • Azoxymethane