Twist as a new prognostic marker in hematological malignancies

Norozi, Fatemeh; Ahmadzadeh, Ahmad; Shahjahani, Mohammad; Shahrabi, Saeid; Saki, Najmaldin

doi:10.1007/s12094-015-1357-0

Cited by 22 publications

(21 citation statements)

References 133 publications

(176 reference statements)

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“…Hypomethylating agents are able to demethylate Wnt antagonist gene promoters in vitro [ 147 ], leading to Wnt reexpression and normal myelopoiesis restoration. Similar results were described for the above mentioned gene TWIST, implicated in the pathophysiology of clonal myeloid diseases [ 148 ], whose reexpression in vitro occurred after treatment with hypomethylating agents [ 149 ]. Regarding autophagy, which confers a sort of cell protection in lower risk MDS and becomes defective along with disease progression, it could be another possible target for hypomethylating agents.…”

Section: Mesenchymal Stem Cells: Therapeutic Implicationssupporting

confidence: 82%

Mesenchymal Stem Cells in Myeloid Malignancies: A Focus on Immune Escaping and Therapeutic Implications

Fracchiolla

Fattizzo

Cortelezzi

2017

Stem Cells International

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The importance of the bone marrow microenvironment forming the so-called niche in physiologic hemopoiesis is largely known, and recent evidences support the presence of stromal alterations from the molecular to the cytoarchitectural level in hematologic malignancies. Various alterations in cell adhesion, metabolism, cytokine signaling, autophagy, and methylation patterns of tumor-derived mesenchymal stem cells have been demonstrated, contributing to the genesis of a leukemic permissive niche. This niche allows both the ineffective haematopoiesis typical of myelodysplastic syndromes and the differentiation arrest, proliferation advantage, and clone selection which is the hallmark of acute myeloid leukemia. Furthermore, the immune system, both adaptive and innate, encompassing mesenchymal-derived cells, has been shown to take part to the leukemic niche. Here, we critically review the state of art about mesenchymal stem cell role in myelodysplastic syndromes and acute myeloid leukemia, focusing on immune escaping mechanisms as a target for available and future anticancer therapies.

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Section: Mesenchymal Stem Cells: Therapeutic Implicationssupporting

confidence: 82%

Mesenchymal Stem Cells in Myeloid Malignancies: A Focus on Immune Escaping and Therapeutic Implications

Fracchiolla

Fattizzo

Cortelezzi

2017

Stem Cells International

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“…Expression of TWIST TFs can induce the EMT process and they are upregulated during cancer development (85,86) and progression to metastasis (87). TWIST TFs are also associated with worse patient prognosis (87).…”

Section: Basic Helix Loop Helix Emt-tfs Twist1 and Twist2mentioning

confidence: 99%

EMT Factors and Metabolic Pathways in Cancer

Georgakopoulos-Soares

et al. 2020

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The epithelial-mesenchymal transition (EMT) represents a biological program during which epithelial cells lose their cell identity and acquire a mesenchymal phenotype. EMT is normally observed during organismal development, wound healing and tissue fibrosis. However, this process can be hijacked by cancer cells and is often associated with resistance to apoptosis, acquisition of tissue invasiveness, cancer stem cell characteristics, and cancer treatment resistance. It is becoming evident that EMT is a complex, multifactorial spectrum, often involving episodic, transient or partial events. Multiple factors have been causally implicated in EMT including transcription factors (e.g., SNAIL, TWIST, ZEB), epigenetic modifications, microRNAs (e.g., miR-200 family) and more recently, long non-coding RNAs. However, the relevance of metabolic pathways in EMT is only recently being recognized. Importantly, alterations in key metabolic pathways affect cancer development and progression. In this review, we report the roles of key EMT factors and describe their interactions and interconnectedness. We introduce metabolic pathways that are involved in EMT, including glycolysis, the TCA cycle, lipid and amino acid metabolism, and characterize the relationship between EMT factors and cancer metabolism. Finally, we present therapeutic opportunities involving EMT, with particular focus on cancer metabolic pathways.

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“…They are able to form homo- and heterodimers with each other [ 146 , 147 , 148 , 149 ] and to directly interact with a large set of transcription factors. The Twist factors are overexpressed in most in human cancers and in most cases correlate with high tumor grade, invasiveness, and metastasis [ 150 , 151 , 152 , 153 , 154 , 155 , 156 ].…”

Section: Transcription Factors In Emt Regulationmentioning

confidence: 99%

MicroRNA Regulation of Epithelial to Mesenchymal Transition

Abba

Patil

Leupold

et al. 2016

JCM

104

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Epithelial to mesenchymal transition (EMT) is a central regulatory program that is similar in many aspects to several steps of embryonic morphogenesis. In addition to its physiological role in tissue repair and wound healing, EMT contributes to chemo resistance, metastatic dissemination and fibrosis, amongst others. Classically, the morphological change from epithelial to mesenchymal phenotype is characterized by the appearance or loss of a group of proteins which have come to be recognized as markers of the EMT process. As with all proteins, these molecules are controlled at the transcriptional and translational level by transcription factors and microRNAs, respectively. A group of developmental transcription factors form the backbone of the EMT cascade and a large body of evidence shows that microRNAs are heavily involved in the successful coordination of mesenchymal transformation and vice versa, either by suppressing the expression of different groups of transcription factors, or otherwise acting as their functional mediators in orchestrating EMT. This article dissects the contribution of microRNAs to EMT and analyzes the molecular basis for their roles in this cellular process. Here, we emphasize their interaction with core transcription factors like the zinc finger enhancer (E)-box binding homeobox (ZEB), Snail and Twist families as well as some pluripotency transcription factors.

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Twist as a new prognostic marker in hematological malignancies

Cited by 22 publications

References 133 publications

Mesenchymal Stem Cells in Myeloid Malignancies: A Focus on Immune Escaping and Therapeutic Implications

Mesenchymal Stem Cells in Myeloid Malignancies: A Focus on Immune Escaping and Therapeutic Implications

EMT Factors and Metabolic Pathways in Cancer

MicroRNA Regulation of Epithelial to Mesenchymal Transition

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