ASPM facilitates colorectal cancer cells migration and invasion by enhancing β-catenin expression and nuclear translocation

Kaohsiung J Med Sci. 2022 Feb;38(2):129-138. doi: 10.1002/kjm2.12464. Epub 2021 Nov 6.

Abstract

Increased abnormal spindle-like microcephaly (ASPM) expression has been linked to clinical stage and poor prognosis in cancers, but the molecular mechanisms by which ASPM promotes cell metastasis in colorectal cancer (CRC) has not been identified. This study showed that the abilities of cell migration, invasion, and epithelial-mesenchymal transition (EMT) were attenuated in ASPM-deficient CRC cell lines. Furthermore, we reported that attenuation of ASPM expression inhibited CRC cell metastasis in vivo. Additionally, the expression of ASPM was positively correlated with β-catenin level in CRC tissues. Mechanistically, ASPM can upregulate β-catenin transcription by stimulating the β-catenin promoter and enhancing the nuclear translocation of β-catenin in CRC cells, which leads to the activation of the Wnt/β-catenin pathway. Finally, we showed that ASPM effectively induced CRC cell migration and invasion in a β-catenin-dependent manner.

Keywords: ASPM; colon cancer; invasion; migration; β-catenin.

MeSH terms

  • Cell Movement*
  • Cell Nucleus
  • Colorectal Neoplasms / metabolism*
  • Colorectal Neoplasms / pathology*
  • Humans
  • Neoplasm Invasiveness
  • Nerve Tissue Proteins / physiology*
  • Protein Transport
  • Tumor Cells, Cultured
  • beta Catenin / biosynthesis*

Substances

  • ASPM protein, human
  • CTNNB1 protein, human
  • Nerve Tissue Proteins
  • beta Catenin