Normal processes of embryonic development and abnormal transformation to cancer have many parallels, and in fact many aberrant cancer cell capabilities are embryonic traits restored in a distorted, unorganized way. Some of these capabilities are cell autonomous, such as proliferation and resisting apoptosis, while others involve a complex interplay with other cells that drives significant changes in neighboring cells. The correlation between embryonic development and cancer is driven by shared proteins. Some embryonic proteins disappear after embryogenesis in adult differentiated cells and are restored in cancer, while others are retained in adult cells, acquiring new functions upon transformation to cancer. Many embryonic factors embraced by cancer cells are transcription factors; some are master regulators that play a major role in determining cell fate. The paired box (PAX) domain family of developmental transcription factors includes nine members involved in differentiation of various organs. All paired box domain proteins are involved in different cancer types carrying pro-tumorigenic or anti-tumorigenic roles. This review focuses on PAX8, a master regulator of transcription in embryonic development of the thyroid, kidney, and male and female genital tracts. We detail the role of PAX8 in each of these organ systems, describe its role during development and in the adult if known, and highlight its pro-tumorigenic role in cancers that emerge from PAX8 expressing organs.
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http://dx.doi.org/10.3390/ijms23137410 | DOI Listing |
PLoS Genet
January 2025
MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, United Kingdom.
The genetic circuitry that encodes the developmental programme of mammals is regulated by transcription factors and chromatin modifiers. During early gestation, the three embryonic germ layers are established in a process termed gastrulation. The impact of deleterious mutations in chromatin modifiers such as the polycomb proteins manifests during gastrulation, leading to early developmental failure and lethality in mouse models.
View Article and Find Full Text PDFPLoS One
January 2025
Ambulatory Healthcare Services, Academic Affairs, Abu Dhabi Health Services (SEHA), Abu Dhabi, UAE.
Background: Non-adherence to cardiovascular medications is a global problem with clinical, economic, and humanistic consequences. Investigation of this problem may open the road for proper management of cardiovascular diseases.
Objective: Our objectives were to assess the level of adherence to, and to examine factors influencing adherence to, cardiovascular medications in subjects visiting a heart center in Sudan.
Biol Reprod
January 2025
Department of Animal Sciences, Genetics Institute, University of Florida, Gainesville, FL, USA.
In vitro fertilization (IVF) is a widely used assisted reproductive technology to achieve a successful pregnancy. However, the acquisition of oxidative stress in embryo in vitro culture impairs its competence. Here, we demonstrated that a nuclear coding gene, methyltransferase-like protein 7A (METTL7A), improves the developmental potential of bovine embryos.
View Article and Find Full Text PDFFront Bioinform
January 2025
Department of Biology and Chemistry, College of Sciences, National University of Defense Technology, Changsha, Hunan, China.
The precise role of lncRNAs in skeletal muscle development and atrophy remain elusive. We conducted a bioinformatic analysis of 26 GEO datasets from mouse studies, encompassing embryonic development, postnatal growth, regeneration, cell proliferation, and differentiation, using R and relevant packages (limma et al.).
View Article and Find Full Text PDFFront Immunol
January 2025
Integrative Immunobiology Department, Duke University, Durham, NC, United States.
Introduction: The regulation of expression during T-cell development and immune responses is essential for proper lineage commitment and function in the periphery. However, the mechanisms of genetic and epigenetic regulation are complex, and their interplay not entirely understood. Previously, we demonstrated the need for CD4 upregulation during positive selection to ensure faithful commitment of MHC-II-restricted T cells to the CD4 lineage.
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