4.6 Article

Epigenetic Regulation of CDH1 Is Altered after HOXB7-Silencing in MDA-MB-468 Triple-Negative Breast Cancer Cells

期刊

GENES
卷 12, 期 10, 页码 -

出版社

MDPI
DOI: 10.3390/genes12101575

关键词

HOXB7; breast cancer; triple-negative; MDA-MB-468; methylation

资金

  1. FEDER (Fundo Europeu de Desenvolvimento Regional) funds through the COMPETE 2020 Operational Programme for Competitiveness and Internationalisation [POCI-01-0145-FEDER-030562]
  2. Portugal 2020
  3. Portuguese funds through FCT (Fundacao para a Ciencia e a Tecnologia/Ministerio da Ciencia, Tecnologia e Ensino Superior) [PTDC/BTM-TEC/30562/2017]
  4. Fundação para a Ciência e a Tecnologia [PTDC/BTM-TEC/30562/2017] Funding Source: FCT

向作者/读者索取更多资源

HOXB7 is often overexpressed in breast cancer cells and related to poor prognosis. Silencing HOXB7 in TNBC cells can lead to lower migration and invasion rates, as well as changes in CDH1 expression and DNA methylation, suggesting a potential therapeutic target for TNBC treatment.
HOXB7 is often overexpressed in breast cancer cells and found to relate to poor prognosis. The search for the HOXB7 targets, as a transcription factor, has led to molecules involved in regulating cell proliferation, migration, invasion, and processes such as angiogenesis and therapy resistance. However, the specific targets affected by the deregulation of HOXB7 in breast cancer remain largely unknown in most molecular sub-types, such as triple-negative breast cancers (TNBC). To unveil the molecular basis behind these aggressive and often untreatable cancers, here we explored the contribution of HOXB7 deregulation for their aggressiveness. To this end, HOXB7 was silenced in TNBC Basal A cells MDA-MB-468, and the phenotype, gene/protein expression, and methylation profile of putative targets were analyzed. Lower migration and invasion rates were detected in HOXB7-silenced cells in comparison with the controls. In addition, these cells expressed more CDH1 and less DNMT3B, and the promoter methylation status of CDH1 diminished. Our data suggest that the HOXB7 transcription factor may act on TNBC Basal A cells by controlling CDH1 epigenetic regulation. This may occur indirectly through the up-regulation of DNMT3B, which then controls DNA methylation of the CDH1 promoter. Thus, future approaches interfering with HOXB7 regulation may be promising therapeutic strategies in TNBC treatment.

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