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TRPS1 Suppresses Breast Cancer Epithelial-mesenchymal Transition Program as a Negative Regulator of SUZ12

Jing Hu1, Peng Su2, Meng Jiao1

  • 1Department of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.

Translational Oncology
|February 23, 2018
PubMed

Insights

Transcriptional repressor GATA binding 1 (TRPS1) inhibits breast cancer (BC) metastasis by suppressing SUZ12. Loss of TRPS1 increases SUZ12, leading to E-cadherin repression and promoting BC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Breast cancer (BC) metastasis remains a significant challenge in treatment.
  • The epithelial-mesenchymal transition (EMT) program is crucial for cancer metastasis.
  • Transcriptional repressor GATA binding 1 (TRPS1) is implicated in primary BC development and progression.

Purpose of the Study:

  • To elucidate the mechanisms by which TRPS1 influences the metastatic cascade in breast cancer.
  • To identify novel targets of TRPS1 involved in BC metastasis and EMT.

Main Methods:

  • Analysis of public breast cancer datasets.
  • In vitro functional studies assessing cell migration and EMT.
  • Bioinformatics analysis and Chromatin Immunoprecipitation (ChIP) assays.
  • Investigation of SUZ12 and E-cadherin regulation.

Main Results:

  • TRPS1 expression loss correlates with higher BC histological grade and increased metastasis.
  • TRPS1 was found to inhibit BC cell migration and EMT.
  • TRPS1 directly represses SUZ12 transcription.
  • Loss of TRPS1 leads to increased SUZ12 binding and H3K27 tri-methylation at the CDH1 promoter, causing E-cadherin repression.

Conclusions:

  • TRPS1 maintains E-cadherin expression by inhibiting SUZ12, thus suppressing BC metastasis.
  • The TRPS1-SUZ12-E-cadherin axis offers new insights into BC progression.
  • Targeting this pathway may present novel therapeutic strategies for metastatic breast cancer.

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