Is There an Interconnection between Epithelial–Mesenchymal Transition (EMT) and Telomere Shortening in Aging?

Abstract

Epithelial–Mesenchymal Transition (EMT) was first discovered during the transition of cells from the primitive streak during embryogenesis in chicks. It was later discovered that EMT holds greater potential in areas other than the early development of cells and tissues since it also plays a vital role in wound healing and cancer development. EMT can be classified into three types based on physiological functions. EMT type 3, which involves neoplastic development and metastasis, has been the most thoroughly explored. As EMT is often found in cancer stem cells, most research has focused on its association with other factors involving cancer progression, including telomeres. However, as telomeres are also mainly involved in aging, any possible interaction between the two would be worth noting, especially as telomere dysfunction also contributes to cancer and other age-related diseases. Ascertaining the balance between degeneration and cancer development is crucial in cell biology, in which telomeres function as a key regulator between the two extremes. The essential roles that EMT and telomere protection have in aging reveal a potential mutual interaction that has not yet been explored, and which could be used in disease therapy. In this review, the known functions of EMT and telomeres in aging are discussed and their potential interaction in age-related diseases is highlighted.

Aged Lens Epithelial Cells Suppress Proliferation and Epithelial–Mesenchymal Transition-Relevance for Posterior Capsule Opacification

“…An EMT suppressive behavior in aged LECs is contrary to epithelial or endothelial cells from many tissues that have been shown to acquire EMT characteristics during aging, which adversely cause organ fibrosis via altering epithelial or endothelial cell phenotypic properties and depositing extracellular matrix (ECM). This includes kidney, cardiac, and idiopathic pulmonary fibrosis [45][46][47][48][49]. We found that hundreds of EMT-promoting genes, including several key EMT markers, such as fibronectin and αSMA, were significantly downregulated.…”

Loxl2 is a mediator of cardiac aging in Drosophila melanogaster, genetically examining the role of aging clock genes

“…Our data suggest that Loxl’s action as a transcriptional regulator may be conserved, which we can now explore in more detail utilizing the advantages of the Drosophila genetic system ( McGuire et al 2004 ; Allocca et al 2018 ; Heigwer et al 2018 ). Loxl2’s known interactions indicate that its role in aging could be through EMT which involves a transitional state that may be partially activated during aging ( Brabletz et al 2018 ) and interestingly EMT is even being pursued in age-related telomere shortening ( Imran et al 2021 ). Further investigation into the extent Loxl2 regulation in the ECM and EMT pathways in Drosophila plays with age, particularly the molecular partners and signaling of Loxl2 in the ECM and nucleus, can now be genetically explored in Drosophila .…”

Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma

“…Type 1 is necessary for the transformation of primitive embryonic epithelial cells into motile mesenchymal cells, which are necessary for neural crest cell gastrulation and migration. Type 1 EMT plays a critical role throughout embryogenesis in generating morphologically and functionally diverse cell types [37]. EMT type 2 causes the development of excessive fibrosis during wound healing and tissue regeneration [38].…”