Wnt3a suppresses Wnt/β-catenin signaling and cancer cell proliferation following serum deprivation

Exp Cell Res. 2016 Feb 1;341(1):32-41. doi: 10.1016/j.yexcr.2015.11.025. Epub 2015 Nov 28.

Abstract

Canonical Wnt/β-catenin signaling is often aberrantly activated in tumor cells and required for tumor growth. The internalization of Wnt co-receptor low-density lipoprotein receptor-related protein 6 (LRP6) induced by Wnt ligands is commonly thought to be critical for Wnt/β-catenin signaling activation. However, in contrast to theses previous studies, we here show that persistent excessive stimulation with a canonical Wnt ligand Wnt3a could induce a long-term decreased expression level of membrane LRP6, which prevented nuclear β-catenin accumulation and tumor cell;proliferation. Importantly, Wnt3a was robustly upregulated following serum deprivation. The upregulated Wnt3a under serum deprivation was responsible for LRP6 internalization, decreased accumulation of nuclear β-catenin, and further inhibition of tumor cell proliferation. It has well been known that insufficient blood supply during tumor development occurs frequently, causing a worsening environment for tumor growth. Therefore, these results reveal a novel inhibitory role of Wnt3a on canonical Wnt/β-catenin signaling and cancer cell proliferation when there is an insufficient blood supply during tumor development, which might be a potential mechanism for tumor evasion within a worsening environment.

Keywords: Cancer cell; Proliferation; Serum deprivation; Wnt/β-catenin; Wnt3a.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation / drug effects
  • Culture Media, Serum-Free / pharmacology*
  • Hep G2 Cells
  • Humans
  • Neoplasms / metabolism*
  • Neoplasms / pathology*
  • Wnt Signaling Pathway* / drug effects
  • Wnt3A Protein / metabolism*
  • beta Catenin / metabolism*

Substances

  • Culture Media, Serum-Free
  • WNT3A protein, human
  • Wnt3A Protein
  • beta Catenin