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TET1 suppresses colon cancer proliferation by impairing β-catenin signal pathway

Hailong Guo1, Hongyi Zhu1, Jie Zhang1

  • 1Department of General Surgery, The Southern Division of Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Cellular Biochemistry
|March 3, 2019
PubMed

Insights

Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) suppresses colon cancer proliferation. Downregulated TET1 promotes tumor growth by upregulating β-catenin signaling in a manner dependent on axis inhibition protein 1 (AXIN1).

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • The role of ten-eleven translocation methylcytosine dioxygenase 1 (TET1) in cancer is context-dependent, with limited research on its function in DNA methylation-sensitive colon cancer.
  • TET1 is involved in active DNA demethylation, a process crucial for epigenetic regulation in cellular functions and disease.

Purpose of the Study:

  • To investigate the role of TET1 in colon cancer proliferation and its underlying molecular mechanisms.
  • To determine the relationship between TET1 expression, the β-catenin pathway, and colon tumorigenesis.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess TET1 expression in colon cancer samples and cell lines.
  • Cell viability assays (MTT and cell count) and in vivo tumor growth studies in mice to evaluate the impact of TET1 modulation.
  • Western blotting and luciferase assays to analyze the activity of the β-catenin (CTNNB1) and WNT signaling pathways.
  • Manipulation of TET1 and axis inhibition protein 1 (AXIN1) expression using short hairpin RNA (shRNA) and transfection.

Main Results:

  • TET1 expression was downregulated in colon cancer tissues and cell lines (HT29, HCT116, SW48).
  • Reduced TET1 expression (shTET1) increased colon cancer cell viability, tumor volume, and tumor weight in mice, accompanied by elevated β-catenin levels and WNT activity.
  • Overexpression of β-catenin rescued diminished cell growth caused by normal TET1 expression.
  • Knockdown of TET1 promoted AXIN1 expression, and inhibiting AXIN1 attenuated the proliferative effects of TET1 knockdown.

Conclusions:

  • TET1 acts as a tumor suppressor in colon cancer, inhibiting cell proliferation.
  • TET1 suppresses colon cancer growth through the inhibition of the β-catenin pathway, which is dependent on AXIN1.
Keywords:
axis inhibition protein1 (AXIN1)colon cancerdemethylationten-eleven translocation methylcytosine dioxygenase 1 (TET1)β-catenin

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