Epigenetic reprogramming and post-transcriptional regulation during the epithelial–mesenchymal transition

Wu, Chung-Yin; Tsai, Ya-Ping; Wu, Min-Zu; Teng, Shu-Chun; Wu, Kou-Juey

doi:10.1016/j.tig.2012.05.005

Cited by 143 publications

(128 citation statements)

References 97 publications

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“…S6). These differences could be because of a couple of possibilities: (1) The process of EMT involves a number of stages (59,60). Although HeLa cells are carcinogenic, they can still, under specific conditions, undergo further EMT (Fig.…”

Section: Transformation Of Cells By Low-dose Chronic Exposure Tomentioning

confidence: 99%

Quantitative Mass Spectrometry Reveals Changes in Histone H2B Variants as Cells Undergo Inorganic Arsenic-Mediated Cellular Transformation

Rea

Eleazer

Eckstein

et al. 2016

Molecular & Cellular Proteomics

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Exposure to inorganic arsenic, a ubiquitous environmental toxic metalloid, leads to carcinogenesis. However, the mechanism is unknown. Several studies have shown that inorganic arsenic exposure alters specific gene expression patterns, possibly through alterations in chromatin structure. While most studies on understanding the mechanism of chromatin-mediated gene regulation have focused on histone post-translational modifications, the role of histone variants remains largely unknown. Incorporation of histone variants alters the functional properties of chromatin. To understand the global dynamics of chromatin structure and function in arsenic-mediated carcinogenesis, analysis of the histone variants incorporated into the nucleosome and their covalent modifications is required. Here we report the first global mass spectrometric analysis of histone H2B variants as cells undergo arsenic-mediated epithelial to mesenchymal transition. We used electron capture dissociation-based top-down tandem mass spectrometry analysis validated with quantitative reverse transcription real-time polymerase chain reaction to identify changes in the expression levels of H2B variants in inorganic arsenic-mediated epithelial-mesenchymal transition. We identified changes in the expression levels of specific histone H2B variants in two cell types, which are dependent on dose and length of exposure of inorganic arsenic. In particular, we found increases in H2B variants H2B1H/1K/1C/1J/1O and H2B2E/2F, and significant decreases in H2B1N/1D/1B as cells undergo inorganic arsenic-mediated epithelial-mesenchymal transition. The analysis of these histone vari-

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Section: Transformation Of Cells By Low-dose Chronic Exposure Tomentioning

confidence: 99%

Quantitative Mass Spectrometry Reveals Changes in Histone H2B Variants as Cells Undergo Inorganic Arsenic-Mediated Cellular Transformation

Rea

Eleazer

Eckstein

et al. 2016

Molecular & Cellular Proteomics

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“…In addition, the cell type-specific regulation of gene expression likely depends on methylation within the CpG context (10). Accumulating evidence demonstrates that abnormal DNA methylation is involved in cancer progression in various human cancers (11)(12)(13). Recently, Dunwell et al (14) screened out FOXF2 as a candidate frequently methylated gene in childhood acute lymphoblastic leukemia samples and cell lines as well as in multiple epithelial cancer cell lines.…”

Section: Foxf2 (Forkhead Box F2mentioning

confidence: 99%

DNA Methylation Affects the SP1-regulated Transcription of FOXF2 in Breast Cancer Cells

Tian

Lun

Huang

et al. 2015

Journal of Biological Chemistry

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Background: Promoter hypermethylation affects the regulation of transcription factors for target genes. Results: SP1 activates FOXF2 transcription, but this activation is prevented through FOXF2 promoter methylation. Conclusion: FOXF2 transcription is regulated through the combined effects of DNA methylation and SP1 transcriptional regulation. Significance: Herein, we describe a new regulatory mechanism for the subtype-specific expression of FOXF2 in breast cancer.

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“…In recent years, there has been a keen interest in understanding the epigenetic regulation during EMT (reviewed in Ref. 99,100 ). Several studies have shown that genome-wide epigenetic changes occur during EMT in response to TGFb (Fig.…”

Section: Epigenetic Rewiring and Noncoding Rnas In Emtmentioning

confidence: 99%

Reprogramming during epithelial to mesenchymal transition under the control of TGFβ

Tan¹,

Olsson

Moustakas

2014

Cell Adhesion & Migration

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Epithelial-mesenchymal transition (EMT) refers to plastic changes in epithelial tissue architecture. Breast cancer stromal cells provide secreted molecules, such as transforming growth factor b (TGFb), that promote EMT on tumor cells to facilitate breast cancer cell invasion, stemness and metastasis. TGFb signaling is considered to be abnormal in the context of cancer development; however, TGFb acting on breast cancer EMT resembles physiological signaling during embryonic development, when EMT generates or patterns new tissues. Interestingly, while EMT promotes metastatic fate, successful metastatic colonization seems to require the inverse process of mesenchymal-epithelial transition (MET). EMT and MET are interconnected in a timedependent and tissue context-dependent manner and are coordinated by TGFb, other extracellular proteins, intracellular signaling cascades, non-coding RNAs and chromatin-based molecular alterations. Research on breast cancer EMT/MET aims at delivering biomolecules that can be used diagnostically in cancer pathology and possibly provide ideas for how to improve breast cancer therapy.

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Epigenetic reprogramming and post-transcriptional regulation during the epithelial–mesenchymal transition

Cited by 143 publications

References 97 publications

Quantitative Mass Spectrometry Reveals Changes in Histone H2B Variants as Cells Undergo Inorganic Arsenic-Mediated Cellular Transformation

Quantitative Mass Spectrometry Reveals Changes in Histone H2B Variants as Cells Undergo Inorganic Arsenic-Mediated Cellular Transformation

DNA Methylation Affects the SP1-regulated Transcription of FOXF2 in Breast Cancer Cells

Reprogramming during epithelial to mesenchymal transition under the control of TGFβ

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