# Pinpointing Functionally Relevant miRNAs in Classical Hodgkin Lymphoma Pathogenesis

**Authors:** Yujia Pan, Roza Cengiz, Joost Kluiver, Arjan Diepstra, Anke Van den Berg

PMC · DOI: 10.3390/cancers16061126 · Cancers · 2024-03-12

## TL;DR

This paper reviews how specific miRNAs contribute to the development of classical Hodgkin lymphoma by targeting genes involved in immune evasion and tumor growth.

## Contribution

The study identifies a cHL-specific miRNA signature and highlights novel miRNA–target gene interactions relevant to lymphoma pathogenesis.

## Key findings

- A cHL-specific miRNA signature was generated based on profiling studies.
- Key miRNAs like miR-155-5p and miR-148a-3p target genes involved in B-cell loss and immune evasion.
- The study provides a foundation for future functional studies on miRNA roles in cHL.

## Abstract

We explored how small non-coding RNAs, known as miRNAs, are involved in the pathogenesis of cHL, a lymphoma originating from B cells. While miRNAs have shown broad effects in normal cellular processes and cancers, their contribution to cHL has been less explored. We organized the published human miRNA profiling studies of cHL and selected genes that are crucial for cHL pathogenesis such as those leading to the loss of B-cell phenotypes, immune evasion, and promotion of tumor growth. By providing a detailed analysis of the interactions between these miRNAs and their target genes, our review not only enhances the understanding of cHL molecular mechanisms but also paves the way for further research into how specific miRNAs could be involved in cHL progression.

Classical Hodgkin lymphoma (cHL) is a hematological malignancy of B-cell origin. The tumor cells in cHL are referred to as Hodgkin and Reed–Sternberg (HRS) cells. This review provides an overview of the currently known miRNA–target gene interactions. In addition, we pinpointed other potential regulatory roles of microRNAs (miRNAs) by focusing on genes related to processes relevant for cHL pathogenesis, i.e., loss of B-cell phenotypes, immune evasion, and growth support. A cHL-specific miRNA signature was generated based on the available profiling studies. The interactions relevant for cHL were extracted by comprehensively reviewing the existing studies on validated miRNA–target gene interactions. The miRNAs with potential critical roles included miR-155-5p, miR-148a-3p, miR-181a-5p, miR-200, miR-23a-3p, miR-125a/b, miR-130a-3p, miR-138, and miR-143-3p, which target, amongst others, PU.1, ETS1, HLA-I, PD-L1, and NF-κB component genes. Overall, we provide a comprehensive perspective on the relevant miRNA–target gene interactions which can also serve as a foundation for future functional studies into the specific roles of the selected miRNAs in cHL pathogenesis.

## Linked entities

- **Genes:** SPI1 (Spi-1 proto-oncogene) [NCBI Gene 6688], ETS1 (ETS proto-oncogene 1, transcription factor) [NCBI Gene 2113], CD274 (CD274 molecule) [NCBI Gene 29126], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790]
- **Diseases:** classical Hodgkin lymphoma (MONDO:0009348), cHL (MONDO:0009348)

## Full-text entities

- **Genes:** MIR155 (microRNA 155) [NCBI Gene 406947] {aka MIRN155, miRNA155, mir-155}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, MIR148A (microRNA 148a) [NCBI Gene 406940] {aka MIRN148, MIRN148A, hsa-mir-148, mir-148a}, ETS1 (ETS proto-oncogene 1, transcription factor) [NCBI Gene 2113] {aka ETS-1, EWSR2, c-ets-1, p54}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, SPI1 (Spi-1 proto-oncogene) [NCBI Gene 6688] {aka AGM10, OF, PU.1, SFPI1, SPI-1, SPI-A}, MIR23A (microRNA 23a) [NCBI Gene 407010] {aka MIRN23A, hsa-mir-23a, miRNA23A, mir-23a}
- **Diseases:** hematological malignancy (MESH:D019337), tumor (MESH:D009369), Classical Hodgkin Lymphoma (MESH:D006689), HRS (MESH:C535516)

## Full text

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## Figures

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## References

132 references — full list in the complete paper: https://tomesphere.com/paper/PMC10968648/full.md

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Source: https://tomesphere.com/paper/PMC10968648