Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition

Gabriel G. Malouf, Joseph H. Taube, Yue Lu, Tapasree Roysarkar, Shoghag Panjarian, Marcos R.H. Estecio, Jaroslav Jelinek, Jumpei Yamazaki, Noel J.M. Raynal, Hai Long, Tomomitsu Tahara, Agata Tinnirello, Priyanka Ramachandran, Xiu Ying Zhang, Shoudan Liang, Sendurai A. Mani, Jean Pierre J. Issa

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Epithelial-mesenchymal transition (EMT) is known to promote cellular plasticity during the formation of the mesoderm from epiblasts and the neural crest cells from the neural tube in the developing embryo as well as during adult wound healing [1]. During EMT, epithelial cells lose their epithelial characteristics and acquire mesenchymal morphology, which facilitates cellular dissociation and migration. Similar to embryo development, neoplastic cells have been shown to reactivate EMT leading to cancer metastasis [2]. Induction of EMT is also involved in the development of resistance to cytotoxic chemotherapy and targeted agents [3-5]. In addition, EMT imparts stem cell properties to differentiated cells [6]. Since cancer cells seem to acquire stem cell properties dynamically in response to the tumor microenvironment and become differentiated at distant sites, it has been suggested that major epigenetic remodeling would occur during EMT to facilitate metastasis. Although DNA methylation changes at specific loci have been established during EMT [7,8], changes in the global DNA methylation landscape are not well understood. Indeed, a recent report demonstrated that DNA methylation is largely unchanged during EMT mediated by transforming growth factor beta (TGF-β) [9], while another showed that EMT is associated with specific alterations of gene-related CpG-rich regions [10]. Moreover, another report showed a striking difference in DNA methylation in non-small cell lung cancers between mesenchymal-like tumors and epithelial-like tumors, which display a better prognosis and exhibit greater sensitivity to inhibitors of epidermal growth factor receptor [11].

Original languageEnglish
Title of host publicationCancer Cell Signaling
Subtitle of host publicationTargeting Signaling Pathways Toward Therapeutic Approaches to Cancer
PublisherApple Academic Press
Pages253-288
Number of pages36
ISBN (Electronic)9781482299458
ISBN (Print)9781771880671
DOIs
Publication statusPublished - 01-01-2014

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Epithelial-Mesenchymal Transition
Epigenomics
Tumors
Stem cells
DNA Methylation
Cells
Chemotherapy
Epidermal Growth Factor Receptor
Transforming Growth Factor beta
Plasticity
Genes
Neoplasms
Stem Cells
Neoplasm Metastasis
Germ Layers
Neural Tube
Tumor Microenvironment
Neural Crest
Mesoderm
Non-Small Cell Lung Carcinoma

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Malouf, G. G., Taube, J. H., Lu, Y., Roysarkar, T., Panjarian, S., Estecio, M. R. H., ... Issa, J. P. J. (2014). Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition. In Cancer Cell Signaling: Targeting Signaling Pathways Toward Therapeutic Approaches to Cancer (pp. 253-288). Apple Academic Press. https://doi.org/10.1201/b17138
Malouf, Gabriel G. ; Taube, Joseph H. ; Lu, Yue ; Roysarkar, Tapasree ; Panjarian, Shoghag ; Estecio, Marcos R.H. ; Jelinek, Jaroslav ; Yamazaki, Jumpei ; Raynal, Noel J.M. ; Long, Hai ; Tahara, Tomomitsu ; Tinnirello, Agata ; Ramachandran, Priyanka ; Zhang, Xiu Ying ; Liang, Shoudan ; Mani, Sendurai A. ; Issa, Jean Pierre J. / Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition. Cancer Cell Signaling: Targeting Signaling Pathways Toward Therapeutic Approaches to Cancer. Apple Academic Press, 2014. pp. 253-288
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Malouf, GG, Taube, JH, Lu, Y, Roysarkar, T, Panjarian, S, Estecio, MRH, Jelinek, J, Yamazaki, J, Raynal, NJM, Long, H, Tahara, T, Tinnirello, A, Ramachandran, P, Zhang, XY, Liang, S, Mani, SA & Issa, JPJ 2014, Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition. in Cancer Cell Signaling: Targeting Signaling Pathways Toward Therapeutic Approaches to Cancer. Apple Academic Press, pp. 253-288. https://doi.org/10.1201/b17138

Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition. / Malouf, Gabriel G.; Taube, Joseph H.; Lu, Yue; Roysarkar, Tapasree; Panjarian, Shoghag; Estecio, Marcos R.H.; Jelinek, Jaroslav; Yamazaki, Jumpei; Raynal, Noel J.M.; Long, Hai; Tahara, Tomomitsu; Tinnirello, Agata; Ramachandran, Priyanka; Zhang, Xiu Ying; Liang, Shoudan; Mani, Sendurai A.; Issa, Jean Pierre J.

Cancer Cell Signaling: Targeting Signaling Pathways Toward Therapeutic Approaches to Cancer. Apple Academic Press, 2014. p. 253-288.

Research output: Chapter in Book/Report/Conference proceedingChapter

TY - CHAP

T1 - Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition

AU - Malouf, Gabriel G.

AU - Taube, Joseph H.

AU - Lu, Yue

AU - Roysarkar, Tapasree

AU - Panjarian, Shoghag

AU - Estecio, Marcos R.H.

AU - Jelinek, Jaroslav

AU - Yamazaki, Jumpei

AU - Raynal, Noel J.M.

AU - Long, Hai

AU - Tahara, Tomomitsu

AU - Tinnirello, Agata

AU - Ramachandran, Priyanka

AU - Zhang, Xiu Ying

AU - Liang, Shoudan

AU - Mani, Sendurai A.

AU - Issa, Jean Pierre J.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Epithelial-mesenchymal transition (EMT) is known to promote cellular plasticity during the formation of the mesoderm from epiblasts and the neural crest cells from the neural tube in the developing embryo as well as during adult wound healing [1]. During EMT, epithelial cells lose their epithelial characteristics and acquire mesenchymal morphology, which facilitates cellular dissociation and migration. Similar to embryo development, neoplastic cells have been shown to reactivate EMT leading to cancer metastasis [2]. Induction of EMT is also involved in the development of resistance to cytotoxic chemotherapy and targeted agents [3-5]. In addition, EMT imparts stem cell properties to differentiated cells [6]. Since cancer cells seem to acquire stem cell properties dynamically in response to the tumor microenvironment and become differentiated at distant sites, it has been suggested that major epigenetic remodeling would occur during EMT to facilitate metastasis. Although DNA methylation changes at specific loci have been established during EMT [7,8], changes in the global DNA methylation landscape are not well understood. Indeed, a recent report demonstrated that DNA methylation is largely unchanged during EMT mediated by transforming growth factor beta (TGF-β) [9], while another showed that EMT is associated with specific alterations of gene-related CpG-rich regions [10]. Moreover, another report showed a striking difference in DNA methylation in non-small cell lung cancers between mesenchymal-like tumors and epithelial-like tumors, which display a better prognosis and exhibit greater sensitivity to inhibitors of epidermal growth factor receptor [11].

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Malouf GG, Taube JH, Lu Y, Roysarkar T, Panjarian S, Estecio MRH et al. Architecture of epigenetic reprogramming following twist1-mediated epithelialmesenchymal transition. In Cancer Cell Signaling: Targeting Signaling Pathways Toward Therapeutic Approaches to Cancer. Apple Academic Press. 2014. p. 253-288 https://doi.org/10.1201/b17138