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Functional characterization of Trip10 in cancer cell growth and survival

Chia-Chen Hsu1, Yu-Wei Leu, Min-Jen Tseng

  • 1Human Epigenomics Center, Department of Life Science, Institute of Molecular Biology and Institute of Biomedical Science, National Chung Cheng University, Chia-Yi, Taiwan.

Journal of Biomedical Science
|February 9, 2011
PubMed
Abstract

Insights

Trip10 (also known as CIP4) DNA methylation differs across cancers. Hypermethylation in brain and breast tumors may promote cancer, while hypomethylation in liver cancer suggests a tumor suppressor role for Trip10.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Cdc42-interacting protein-4, Trip10 (CIP4), is a multi-domain adaptor protein with tissue-specific functions.
  • Trip10 is highly expressed in ER+ breast cancer; its depletion increases DNA methylation.
  • Hypothesized Trip10 acts as a tumor suppressor in ER- breast cancer and is epigenetically regulated by DNA methylation in other cancers.

Purpose of the Study:

  • To investigate the epigenetic regulation of Trip10 by DNA methylation in liver, brain, ovarian, and breast cancers.
  • To evaluate the role of Trip10 as a tumor suppressor or oncogene in different cancer types.

Main Methods:

  • Methylation-specific polymerase chain reaction and bisulfite sequencing were used to assess Trip10 DNA methylation.
  • Trip10 was overexpressed to study its effects on cell colony formation and in vivo tumorigenesis.

Main Results:

  • Trip10 was hypermethylated in brain tumors and breast cancer, but hypomethylated in liver cancer.
  • Overexpression of Trip10 promoted colony formation and tumorigenesis in brain tumor (IMR-32) cells.
  • Overexpression of Trip10 suppressed colony formation and tumorigenesis in ovarian cancer (CP70) cells.

Conclusions:

  • Trip10's role in cancer cell growth and death is cancer-type specific.
  • Differential DNA methylation of Trip10 can promote cell survival or cell death depending on the cell type.

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