Journal of Tumour Research & Reports

Role of Epithelial Mesenchymal Transition in Tumour Development and Metastasis

Paul Johnstone^* Department of Pathology, University of Cambridge, Cambridge, UK
^*Correspondence: Paul Johnstone, Department of Pathology, University of Cambridge, Cambridge, UK, Email:

Received: 21-Apr-2022, Manuscript No. JTRR-22-16766; Editor assigned: 25-Apr-2022, Pre QC No. JTRR-22-16766 (PQ); Reviewed: 13-May-2022, QC No. JTRR-22-16766; Revised: 19-Mar-2022, Manuscript No. JTRR-22-16766 (R); Published: 30-May-2022, DOI: 10.35248/2684-1614.22.7.162

Description

Epigenetics is the study of heritable molecular determinants that aren't affected by phenotypic characteristics. DNA methylation, histone alterations, non-coding RNAs, and chromatin remodelling are all epigenetic characteristics. The epigenetic state of a cell determines its differentiation status and capacity to execute its right function in multicellular organisms. These pathways are now widely acknowledged as important contributors to tumour growth and metastasis. Epithelial Mesenchymal Transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. In cancer, EMT is linked to carcinogenesis, invasion, metastasis, and therapeutic resistance. Now we look at recent studies that show the biological role of epigenetics, specifically DNA methylation, histone modifications, non-coding RNAs, and chromatin remodelling, in tumour progression and metastasis by regulating EMT status, and we give an overview of the current state of knowledge about epigenetics and tumour progression and metastasis. Because epigenetic modifications can be reversed, understanding their biological functions in EMT will help us not only better understand how cancer evolves and spreads, but also identify new strategies to diagnose and treat human malignancy, which are now absent in the clinical context. Despite recent advances in the diagnosis and treatment of a range of malignancies, metastasis remains the top cause of death in cancer patients. As cancer grows, it becomes increasingly heterogeneous, leading in the development of aggressive subsets of cancer cells that infiltrate local tissues, lymph vessels, and circulatory systems before spreading throughout the body. The main tumour eventually spreads and metastasizes as a result of the aggressive nature of the original tumour [1,2]. As a result, selecting treatment targets that can be employed to slow or stop cancer growth and progression requires first understanding the mechanism of cancer spreading. Gene mutations and epigenetic alterations, as well as the rewiring of cell signalling and the reprogramming of metabolic pathways, are all part of the process of cell transformation and cancer growth. Furthermore, a large body of research published over the last few decades has demonstrated that epigenetic changes have a role in tumour genesis and progression. It has also been suggested that throughout the growth of cancers, genetic and epigenetic modifications are intimately related [3,4].

DNA methylation, covalent histone modifications, glycosylation, and ubiquitination are all epigenetic processes that regulate tumour cell proliferation and gene expression. In various tumour cells, these epigenetic alterations have varied characteristics and distribution patterns. The epigenome is a major determinant of cell destiny because of the unique pattern of combinations of these alterations. . To maintain an adequate level of differentiation, the epigenetic state within cells is tightly maintained. This fine-tuned genetic programming is disturbed in cancer, resulting in uncontrolled cell proliferation, poor differentiation, and apoptosis resistance. Epigenetic events, such as gene expression stability and genetic alterations, are unrelated to changes in the original DNA sequence. We look at the latest research on the role of epigenetics in metastasis, which could help direct cell spread from the source tumour or eventual growth and colonisation at distant places. This knowledge will help us understand the functional significance of epigenetic processes and provide useful treatment information for cancers that target epigenetic modifications in metastatic cells [5].

Conclusion

Epigenetic control and tumour metastasis play distinct roles in the occurrence and progression of cancers, and associated enzymes and regulatory factors could be used to treat cancer. Despite the fact that no single epigenetic regulator is altered in tumour metastasis, there is accumulating evidence that metastatic tissue has a different epigenetic status than primary tumour tissue, which can be used in cancer therapy and detection. Modulating epigenetic changes and understanding the role of epigenetics in EMT and metastasis will bring fresh insights into our understanding of tumour growth and metastasis due to the nature of epigenetic modifications.

Because epigenetic alterations are reversible, a complete understanding of their role in EMT can reveal novel information about tumour growth and metastasis. It could also help with the development of human cancer diagnostic and therapy procedures. Epigenetic changes linked to EMT are being studied as a potential biomarker in the clinic. Because of the complexities of epigenetic transformation, we must pay close attention to the epigenetic properties of the target protein or RNA when utilizing targeted medications, which implies that our drugs must be more cautious. Nonetheless, we feel that a thorough understanding of the epigenetic features of EMT regulation and metastasis will be a great starting point for the development of predictive cancer biomarkers. Furthermore, the creation of particular inhibitors of enzymatic proteins that are generated by epigenetic modification will offer fresh hope for treating tumour metastasis.

REFERENCES

1. Budi EH, Duan D, Derynck R. Transforming Growth Factor-β Receptors and Smads: Regulatory Complexity and Functional Versatility. Trends Cell Biol. 2017; 27: 658–672.

   [Croosref], [Google scholar], [Pubmed]

2. Dongre A, Weinberg RA. New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nat Rev Mol Cell Biol. 2019; 20: 69–84.

   [Croosref], [Google scholar], [Pubmed]

3. Hobert O. Gene regulation by transcription factors and microRNAs. Science. 2008; 319: 1785–1786.

   [Croosref], [Google scholar],[Pubmed]

4. Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition. J Clin Investig. 2009; 119: 1420–1428.

   [Croosref], [Google scholar], [Pubmed]

5. Zhang Y, Weinberg RA. Epithelial-to-mesenchymal transition in cancer: complexity and opportunities. Front Med. 2018; 12: 361–373.

   [Croosref], [Google scholar], [Pubmed]