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

Translational Oncology
Jing HuBo Han

Abstract

Breast cancer (BC) is among the most common malignant diseases and metastasis is the handcuff of treatment. Cancer metastasis is a multistep process associated with the epithelial-mesenchymal transition (EMT) program. Several studies have demonstrated that transcriptional repressor GATA binding 1 (TRPS1) played important roles in development and progression of primary BC. In this study we sought to identify the mechanisms responsible for this function of TRPS1 in the continuum of the metastatic cascade. Here we described that TRPS1 was significantly associated with BC metastasis using public assessable datasets. Clinically, loss of TRPS1 expression in BC was related to higher histological grade. In vitro functional study and bioinformatics analysis revealed that TRPS1 inhibited cell migration and EMT in BC. Importantly, we identified SUZ12 as a novel target of TRPS1 related to EMT program. ChIP assay demonstrated TRPS1 directly inhibited SUZ12 transcription by binding to the SUZ12 promoter. Loss of TRPS1 resulted in increased SUZ12 binding and H3K27 tri-methylation at the CDH1 promoter and repression of E-cadherin. In all, our data indicated that TRPS1 maintained the expression of E-cadherin by inhibiting SUZ12, which might pro...Continue Reading

Citations

Jun 25, 2020·Cancer Metastasis Reviews·Belinda J Petri, Carolyn M Klinge
Feb 27, 2021·International Journal of Cancer. Journal International Du Cancer·Françoise BeltjensLaurent Arnould
Jan 7, 2022·Journal of Leukocyte Biology·Yingying ChenRong Fu

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Datasets Mentioned

BETA
GSE25066
GSE2990
GSE104062
MDA-MB-453

Methods Mentioned

BETA
Transfection
Immunoprecipitation
PCR
Assay
ChIP
acetylation

Software Mentioned

Kaplan
Genomatrix
Meier Plotter
FIREBROWS
SPSS
JASPAR
GSEA
Graph Pad Prism
Gene Set Enrichment Analysis ( GSEA
PROMO

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