Abstract
Plasma cells (PC) are the main effectors of adaptive immunity, responsible for producing antibodies to defend the body against pathogens. They are the result of a complex highly regulated cell differentiation process, taking place in several anatomical locations and involving unique genetic events. Pathologically, PC can undergo tumorigenesis and cause a group of diseases known as plasma cell dyscrasias, including multiple myeloma (MM). MM is a severe disease with poor prognosis that is characterized by the accumulation of malignant PC within the bone marrow, as well as high clinical and molecular heterogeneity. MM patients frequently develop resistance to treatment, leading to relapse. Polycomb group (PcG) proteins are epigenetic regulators involved in cell fate and carcinogenesis. The emerging roles of PcG in PC differentiation and myelomagenesis position them as potential therapeutic targets in MM. Here, we focus on the roles of PcG proteins in normal and malignant plasma cells, as well as their therapeutic implications.
Highlights
Since the end of the 19th century, plasma cells (PC) have been a major topic of research in order to understand their function and origin [1]
We summarize the current knowledge on Polycomb group (PcG) protein implication in PC differentiation, myelomagenesis, and MM pathophysiology
One of the important points in the biology of PcG proteins is that none of the core members of polycomb repressive complex 1 (PRC1) or polycomb repressive complex 2 (PRC2) can recognize specific DNA sequences on their own, and they all need to be recruited by partners to regulate the specific expression of their target genes [8]
Summary
Since the end of the 19th century, plasma cells (PC) have been a major topic of research in order to understand their function and origin [1]. It is established that PC constitute the terminal stage of B lymphocyte differentiation and are the major players of the humoral immune response. Multiple myeloma (MM), a frequent hematologic cancer that in most cases remains untreated, is caused by malignant PC transformation and accumulation in the bone marrow [5]. In this context, many groups are investigating the modulation of the physiological differentiation of PC by epigenetic factors as well as their tumoral transformation. Polycomb group (PcG) proteins are major epigenetic regulators of gene expression during development and cell fate choice. We discuss potential therapeutic options for patients with MM on the basis of these data
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