Expression alternation and function of long non-coding RNAs in NHL cancer

Expression alternation and function of long non-coding RNAs in NHL cancer Non-Hodgkin lymphoma (NHL) encompasses a diverse group of blood cancers characterized by uncontrolled growth of B cells or T cells. Despite significant progress in treatment, NHL continues to pose a substantial global health challenge. In recent years, long non-coding RNAs (lncRNAs) have emerged as significant contributors to cancer development and progression. This review delves into the role of lncRNAs in NHL, with a focus on their altered expression patterns and functional implications. LncRNAs, which are non-coding RNAs longer than ۲۰۰ nucleotides and devoid of protein-coding capacity, play critical roles in various cellular processes, including gene expression regulation, chromatin remodeling, and cellular signaling. They exert their functions through mechanisms such as acting as molecular sponges for microRNAs (miRNAs), forming RNA-protein complexes, and interacting with DNA to regulate chromatin structure. Numerous studies have revealed dysregulated expression of lncRNAs in NHL compared to normal B cells, involving both upregulation and downregulation of specific lncRNAs. For example, lncRNA HOTAIR is frequently overexpressed in NHL, where it fosters tumorigenesis by suppressing the tumor suppressor p۱۵. Conversely, lncRNA MEG۳ is downregulated in NHL and demonstrates tumor-suppressive properties by targeting miR-۱۵۵. LncRNAs play a crucial role in the development and progression of NHL by influencing various mechanisms: Modulating Gene Expression: LncRNAs interact with transcription factors, chromatin-modifying complexes, and other regulatory molecules to modulate gene expression. For example, lncRNA MALAT۱ activates Wnt/β-catenin signaling, promoting tumorigenesis and metastasis in diffuse large B-cell lymphoma. Competing Endogenous RNAs (ceRNAs): LncRNAs act as ceRNAs by competing with mRNAs for binding to miRNAs, thus regulating the expression of target genes. LncRNA H۱۹, for instance, promotes lymphoma progression by sequestering miR-۱۲۵b and miR-۱۴۶a. Splicing Regulation: LncRNAs influence alternative splicing, leading to the production of different protein isoforms with distinct functions. Chromatin Remodeling: LncRNAs interact with chromatin-modifying enzymes to alter chromatin structure and accessibility, affecting gene expression. For example, lncRNA NEAT۱ promotes tumorigenesis and metastasis of follicular lymphoma by activating NF-κB signaling. Understanding the mechanisms underlying lncRNA-mediated regulation in NHL can provide valuable insights into disease pathogenesis and identify potential therapeutic targets. Further research is needed to elucidate the specific functions of individual lncRNAs in NHL and to develop strategies for targeting these molecules for therapeutic intervention.

کلیدواژه ها:

Long Non-Coding RNAs ، Non-Hodgkin Lymphoma ، Gene Expression ، Therapeutic Targets