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Transcriptomic and epigenetic analysis of breast cancer stem cells

  • Guochao Li
  • , Dong Wang
  • , Wencui Ma
  • , Ke An
  • , Zongzhi Liu
  • , Xinyu Wang
  • , Caiyun Yang
  • , Fengxia Du
  • , Xiao Han
  • , Shuang Chang
  • , Hui Yu
  • , Zilong Zhang
  • , Zitong Zhao
  • , Yan Zhang
  • , Junyun Wang*
  • , Yingli Sun
  • *Corresponding author for this work
  • CAS - Beijing Institute of Genomics
  • University of Chinese Academy of Sciences
  • Heze Third People's Hospital
  • Harbin Medical University

Research output: Contribution to journalArticlepeer-review

Abstract

Aim: Cancer stem cells (CSCs) drive triple-negative breast cancer recurrence via their properties of self-renewal, invasiveness and radio/chemotherapy resistance. This study examined how CSCs might sustain these properties. Materials & methods: Transcriptomes, DNA methylomes and histone modifications were compared between CSCs and non CSCs. Results: Transcriptome analysis revealed several pathways that were activated in CSCs, whereas cell cycle regulation pathways were inhibited. Cell development and signaling genes were differentially methylated, with histone methylation analysis suggesting distinct H3K4me2 and H3K27me3 enrichment profiles. An integrated analysis revealed several tumor suppressor genes downregulated in CSCs. Conclusion: Differential activation of various signaling pathways and genes contributes to the tumor-promoting properties of CSCs. Therapeutic targets identified in the analysis may contribute to improving treatment options for patients.

Original languageEnglish
Pages (from-to)765-783
Number of pages19
JournalEpigenomics
Volume10
Issue number6
DOIs
StatePublished - Jun 2018
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • DNA methylation
  • H3K27me3
  • H3K4me2
  • breast cancer stem cells
  • epigenome
  • histone modification
  • multiple omics analysis
  • transcriptome

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