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Biomolecules
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Role of EMT Transcription Factors in Hematopoietic Development, Immune Cell...
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Role of EMT Transcription Factors in Hematopoietic Development, Immune Cell Function and Leukemic Transformation

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 1859

Special Issue Editor

Dr. Jody Jonathan Haigh

E-Mail Website
Guest Editor
1. Department of Pharmacology and Therapeutics, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada
2. CancerCare Manitoba Research Institute, Winnipeg, MB, Canada
Interests: cancer biology; cell fate engineering; epigenetics; hematopoiesis; in vivo disease modeling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Transcription factors (TFs), such as ZEB (ZEB1/2), SNAI (SNAI1-3), and TWIST (TWIST1/2) members, are involved in the regulation of epithelial-to-mesenchymal cell transition (EMT) events associated with a loss of epithelial polarity during developmental processes such as gastrulation and neural crest delamination. From a pathological perspective, these EMT-associated transcription factors (EMT-TFs) can be co-opted to drive cancer cell metastasis and therapy resistance and relapse and enhance cancer stemness properties. These EMT-TFs are not only limited to regulating aspects of epithelial cell pathophysiology but have also been demonstrated to play essential cell-autonomous roles in regulating hematopoietic cell differentiation and immune cell function. Hematopoietic cell lineage mutation and/or dysregulated expression of these EMT-TFs can lead to hematological malignancies and have been implicated in acute myeloid and lymphoid leukemia initiation and progression. Alterations in EMT-TF function are associated with alterations in key epigenetic regulator activity and may represent potential targets for novel cancer therapies. This Special Issue aims to bring together recent primary data articles as well as reviews highlighting advancements in our understanding of the roles that these EMT-TFs play in hematopoietic development, immune cell function, and leukemic transformation. Papers dealing with the role of EMT-TFs in immune cell surveillance and immune checkpoint control in cancer are also welcome.

Dr. Jody Jonathan Haigh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • transcription factors
  • epigenetics
  • hematopoiesis
  • leukemia
  • immune cell function

Published Papers (1 paper)

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Research

11 pages, 1086 KiB  
Article
Zeb1 Regulates the Function of Lympho-Myeloid Primed Progenitors after Transplantation
by Alhomidi Almotiri, Ashleigh S. Boyd and Neil P. Rodrigues
Biomolecules 2023, 13(9), 1386; https://doi.org/10.3390/biom13091386 - 14 Sep 2023
Cited by 1 | Viewed by 1509
Abstract
Zeb1, a zinc finger E-box binding homeobox epithelial–mesenchymal (EMT) transcription factor, acts as a critical regulator of hematopoietic stem cell (HSC) self-renewal and multi-lineage differentiation. Whether Zeb1 directly regulates the function of multi-potent progenitors primed for hematopoietic lineage commitment remains ill defined. [...] Read more.
Zeb1, a zinc finger E-box binding homeobox epithelial–mesenchymal (EMT) transcription factor, acts as a critical regulator of hematopoietic stem cell (HSC) self-renewal and multi-lineage differentiation. Whether Zeb1 directly regulates the function of multi-potent progenitors primed for hematopoietic lineage commitment remains ill defined. By using an inducible Mx-1 Cre conditional mouse model where Zeb1 was genetically engineered to be deficient in the adult hematopoietic system (hereafter Zeb1−/−), we found that the absolute cell number of immunophenotypically defined lympho-myeloid primed progenitors (LMPPs) from Zeb1−/− mice was reduced. Myeloid- and lymphoid-biased HSCs in Zeb1−/− mice were unchanged, implying that defective LMPP generation from Zeb1−/− mice was not directly caused by an imbalance of lineage-biased HSCs. Functional analysis of LMPP from Zeb1−/− mice, as judged by competitive transplantation, revealed an overall reduction in engraftment to hematopoietic organs over 4 weeks, which correlated with minimal T-cell engraftment, reduced B-cell and monocyte/macrophage engraftment, and unperturbed granulocyte engraftment. Thus, Zeb1 regulates LMPP differentiation potential to select lympho-myeloid lineages in the context of transplantation. Full article
(This article belongs to the Special Issue Role of EMT Transcription Factors in Hematopoietic Development, Immune Cell Function and Leukemic Transformation)
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